HEMODYNAMIC ROUNDS

Admixture lesions in congenital cyanotic heart disease

Jaganmohan A Tharakan
Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India

not increase systemic blood flow significantly. When

INTRODUCTION
oxygenated blood mixes with deoxygenated blood (eg.,
Cyanotic congenital heart disease (CCHD) usually VSD), pulmonary blood flow increases and obviously,
portends poor prognosis as it reflects a more complex does not result in cyanosis.
form of congenital heart disease (CHD). Normally, the
Mixing of deoxygenated blood with oxygenated blood,
systemic circulation and pulmonary circulation are
resulting in cyanosis, can occur at the level of the
in series and the entire blood transiting the systemic
systemic veins, atria, ventricles, great vessels, and
circulation finds its way to the pulmonary circulation
at distal pulmonary vascular bed. Let us look at few
and there is no mixing of deoxygenated blood with the
oxygenated blood, except for the bronchial veins that examples of CCHD with a systemic oxygen saturation
drain to pulmonary veins (<3% of the cardiac output). of 85%:
1. Tetralogy of Fallot
Systemic circulation being the dominant circulation, 2. VSD and Eisenmenger syndrome
maintenance of cardiac output and systemic blood 3. Common atrium
pressure take priority for sustenance of life. The role of 4. Tricuspid atresia
pulmonary circulation is oxygenation of blood and plays
5. Simple TGA
a minor role in maintaining overall hemodynamics of
pressures and flows. Though the systemic oxygen saturation is identical,
the underlying hemodynamic abnormalities are vastly
Systemic blood flow (cardiac output) in the basal state
different.
is maintained within a narrow physiological range,
maintaining optimal tissue perfusion pressure through In Tetralogy of Fallot, pulmonary blood flow is reduced
various neurohumoral mechanisms. Pulmonary due to subpulmonic obstruction, facilitating right to left
circulation does not possess such an efficient shunt. In VSD with Eisenmenger syndrome, pulmonary
neurohumoral mechanism to limit the pulmonary blood flow is reduced due to pulmonary vascular disease
blood flow and is normally controlled by the dominant and increased pulmonary impedance, facilitating right
systemic circulation as the two are in series. This is to left shunt. In common atrium, and tricuspid atresia,
exemplified by the circulation in transposition of both admixture lesions, the pulmonary blood flow is
great vessels (TGA) where the two circulations can likely to be normal or mildly increased (equal to or
be described as in parallel. In TGA, the systemic mildly more than systemic blood flow), as the admixture
blood flow is usually in the normal range despite physiology facilitates complete mixing of deoxygenated
hypoxemia, whereas the pulmonary blood flow and oxygenated blood and the arterial saturation is
progressively increases with reduction in pulmonary determined by the contribution of oxygenated blood
vascular resistance and regression of left ventricular
(pulmonary blood flow) to the admixture. In simple TGA,
mass and compliance. Mixing of deoxygenated blood
the pulmonary blood flow has to be significantly more
with oxygenated blood results in cyanosis but does
than systemic blood flow to allow oxygenated blood
to traverse atrial septal defect from left atrium (LA) to
right atrium (RA) and thus improve the systemic oxygen
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saturation which otherwise will have only recirculating
Quick Response Code:
Website: systemic venous blood. This highlights the fact that
www.annalspc.com for varying degrees of pulmonary blood flow, we can
obtain similar systemic arterial saturations and the
DOI: hemodynamic determinants of right to left shunt, and
10.4103/0974-2069.79625 systemic arterial saturation is different in each of these
conditions.

Address for correspondence: Prof. Jaganmohan A Tharakan, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum 695 011, India.
E-mail: jaganmohan.tharakan@gmail.com

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Tharakan: Admixture lesions in CCHD

patient with single ventricle with PS is 90% and systemic

CONGENITAL CYANOTIC HEART DISEASE
saturation is 70%, then pulmonary blood flow to systemic
WITH ADMIXTURE PHYSIOLOGY blood flow ratio is 2 : 1, indicating increased pulmonary
Definition blood flow.

Congenital Cyanotic heart disease (CCHD) with Calculation of pulmonary vascular resistance (PVR)
admixture physiology is a cardiac defect which facilitates requires minute oxygen consumption (VO 2 ) and
complete mixing of the deoxygenated systemic venous hemoglobin concentration, the pulmonary artery (PA)
(SV) blood returning from the tissues and the fully pressure, and pulmonary blood flow.
oxygenated pulmonary venous blood from the lungs in Though the admixture cardiac lesions facilitate complete
a common receiving chamber. mixing in a common chamber, this is often not the
Basic concepts case. This can result in two scenarios. The pulmonary
venous return can preferentially stream into the aorta
As the mixing of the deoxygenated SV blood and the fully
(AO) precluding complete admixture and result in
oxygenated pulmonary venous blood is a simple physical
higher oxygen saturation in the AO than the PA. This
process, the resultant mix of blood will have saturation
is described as favorable streaming. Conversely, the
somewhere in between that of SV and pulmonary venous
pulmonary venous return can selectively enter the
blood oxygen saturation. When mixing is complete,
PA resulting in higher oxygen saturation in PA than
the resultant oxygen saturation will depend on the
AO. This can be described as unfavorable streaming.
relative contribution of the amount of blood from each
Thus, it is apparent that for identical pulmonary blood
circulation. As discussed earlier, the systemic blood flow
flow, the systemic arterial oxygen saturation can vary
is maintained within a narrow physiological range in the
considerably depending on the streaming in the common
basal state. Assuming the cardiac index to be within the
mixing chamber.
normal range, the effective saturation of the completely
admixed blood will be linearly related to the amount The relationship of arterial oxygen saturation to
of oxygenated blood from the lung (pulmonary blood pulmonary blood flow is influenced both by the total
flow).[1] Therefore, the systemic arterial saturation in pulmonary blood flow and the type and degree of
an admixture cardiac defect will reflect the pulmonary streaming in the mixing chamber. Cardiac catheterization
blood flow. and hemodynamic study is often necessary for assessing
PVR and operability.
It is safe to assume that for a normal cardiac index, the
artero-venous oxygen difference will be around 25% in Congenital cyanotic heart disease with admixture
the basal state. In admixture lesions, the aortic saturation physiology
and the pulmonary saturation will be identical. If the
The common CCHD with admixture physiology include
aortic saturation is 85%, PA saturation can be assumed
totally anomalous pulmonary venous connection
as 85% and PV saturation as 100%. If we assume normal
(TAPVC), atresia of one of the atrioventricular valves
cardiac index, then the artero-venous oxygen difference
(Tricuspid atresia, mitral atresia), single ventricle
will be approximately 25%, that is, the SV saturation
physiology (double inlet ventricle), semilunar valve
will be around 60%. QP/QS = (AO saturation - Systemic
atresia (pulmonary atresia including hypoplastic right
venous saturation)/(PV saturation – PA saturation) =
heart syndrome, aortic atresia including hypoplastic
(85-60)/(100 – 85) = 25/15 = 1.67 : 1. left heart syndrome), double outlet RV or double outlet
LV, complete deficiency of atrial septum as in common
Let us assume that SV saturation in the above example is
atrium, and complete deficiency of conotruncal and
70%, indicating a lesser arterio-venous oxygen difference
trunco-aortic septum as in truncus arteriosus.
and also reflecting a higher systemic flow. The Qp/Qs =
(85-70)/100-85 = 15/15 = 1. Common examples of admixture lesions and issues in the
hemodynamic assessment are discussed below:
This example highlights the importance of obtaining
the SV saturation as well as the systemic arterial Double outlet right ventricle
oxygen saturation in calculating flow ratios to compute
The commoner forms of double outlet right ventricle
pulmonary to systemic vascular resistance (SVR) ratio
(DORV) without pulmonary stenosis can have subaortic
and limitations of aortic oxygen saturation taken in
VSD or subpulmonic VSD. Though described as an
isolation as an indicator of pulmonary blood flow. For
admixture lesion, RV acting as the mixing chamber,
identical aortic oxygen saturation, reducing SV saturation
often complete mixing does not occur. The LV pumps
will in effect increase the calculated pulmonary to
into the great vessels, using RV as a conduit and little
systemic blood flow ratio.
opportunity to effect complete mixing in RV. Incomplete
Applying the same logic, if the aortic saturation in a mixing or streaming is commonly seen in DORV. In DORV

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 Tharakan: Admixture lesions in CCHD

with subaortic VSD, LV blood preferentially enters the IVC can selectively stream into the LA across the ASD
AO and RV blood enters the PA, resulting in favorable (favorable streaming). This can result in dissimilar
streaming and aortic oxygen saturation significantly saturation in AO and PA. Thus, low arterial oxygen
higher than PA. When the VSD is subpulmonic in location, saturation can be due to reduced pulmonary blood flow
the LV blood preferentially enters the PA and the RV due to pulmonary vascular disease, or PV desaturation
blood preferentially enters the AO. This is unfavorable due to pulmonary venous channel obstruction, or due to
streaming with PA saturation more than the AO. In effect, passive pulmonary hypertension secondary to pulmonary
DORV with subaortic VSD presents like a large left to venous hypertension, or due to unfavorable streaming.
right shunt VSD, as the desaturation is mild and cyanosis Conversely, infradiaphragmatic obstructed TAPVC can
inapparent. DORV with subpulmonic VSD presents maintain fair systemic saturation despite being moribund
clinically as TGA with VSD, with significant systemic due to PVH and pulmonary edema (unfavorable anatomy,
desaturation and cyanosis despite increased pulmonary but favorable streaming).[6]
blood flow. The same argument is appropriate for DORV
Interestingly, when TAPVC is associated with conditions
with pulmonic stenosis. Though DORV is an admixture
like pulmonary atresia and complete endocardial cushion
lesion, due to variable streaming of blood, the systemic
defect as in visceral heterotaxy (two admixture lesions in
saturation may not accurately reflect the pulmonary
tandem), the clinical picture is dominated by the second
blood flow, and hemodynamic study is often necessary
lesion and TAPVC may be overlooked unless special care
to assess pulmonary blood flow and resistance.[2-4]
is taken to identify the pulmonary venous drainage. This
Total anomalous pulmonary venous drainage or is important when Glenn shunt is planned as TAPVC will
connection interfere with rerouting of SVC to PA.

Regardless of the site of drainage of the pulmonary When TAPVC, an admixture lesion, is associated with
veins (PVs), the RA acts as an effective mixing chamber. TGA, it may be beneficial as complete admixture of
Typically, the RA, RV, PA, LA, LV, and aortic oxygen oxygenated and deoxygenated blood will mitigate issues
saturation will be identical. This will also mask any shunt of lack of mixing, so characteristic of TGA.
downstream from the RA, as the saturations are identical
In the other pretricuspid admixture lesions, like common
in the upstream chambers, RA, and LA and additional step
atrium, TAPVC to RA and tricuspid atresia, streaming has
up or step down in saturation cannot occur. Assuming
not been well characterized.
complete admixture and assuming normal systemic
cardiac output, the aortic saturation will indirectly Single ventricle
reflect the pulmonary blood flow.[1] Alternately, if the In single-ventricle physiology with two patent AV valves,
aortic saturation is very low, then it indirectly indicates both favorable and unfavorable streaming is often seen
decreased pulmonary blood flow and hence pulmonary and does not necessarily depend on the ventricular
vascular disease. Conversely, if the pulmonary blood morphology or the great vessel relation. Some patients
flow is markedly increased, then the aortic saturations with DILV with aorta arising from the left-sided and
can be as high as 90% and cyanosis may be missed. It anterior rudimentary RV outflow chamber (inverted)
is not uncommon to make a clinical diagnosis of ASD have “favorable streaming,” with SV blood preferentially
as all other clinical features are like a large left to right directed into the PA and pulmonary venous return
shunt ASD and the minimal cyanosis can be missed.[5] It directed to the aorta. Similarly, patients with aorta
should be noted that only a minority of TAPVC remain from a right-sided and anterior rudimentary RV outflow
asymptomatic and present like an ASD, as majority chamber (non-inverted) may have “unfavorable”
will have some anatomic or functional obstruction to streaming.[7,8]
the anomalous channel resulting in pulmonary venous
hypertension early in life. Only 50% of TAPVC survive Patients with univentricular hearts characteristically
have a complete mix of systemic and pulmonary venous
3 months and 20% survive one year without surgery.
circulations at the ventricular level. If one assumes
Streaming in TAPVC: In fetal circulation, the IVC blood is a pulmonary venous oxygen saturation of 100% and
directed to the atrial septum and the fossa to LA, while the normal systemic blood flow (cardiac output), the arterial
SVC blood is directed to the tricuspid valve (TV) and RV. oxygen saturation will reflect pulmonary blood flow. As a
Similarly, the direction of flow from the coronary sinus is rule of thumb, values 85% and <75% signify increased
away from the fossa and toward the TV. This physiological and decreased pulmonary blood flow, respectively.
streaming is maintained to some extent in the postnatal
Truncus arteriosus
life when there is an associated TAPVC. Supracardiac
TAPVC draining into SVC or to coronary sinus can stream Streaming is well documented in truncus arteriosus and
selectively to the TV, RV, and into PA (unfavorable can result in substantial difference in aortic and pulmonary
streaming) and infradiaphragmatic TAPVC draining to arterial saturation. This should caution us when we use

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Tharakan: Admixture lesions in CCHD

systemic arterial saturation as indicator of pulmonary SVR ratio <0.7) may be offered surgery even when the
blood flow and pulmonary vascular disease.[9-11] PA and aortic systolic pressure are identical.[13,14]
Hypoplastic left heart syndrome The patients with near-normal PA pressures are generally
those with pulmonary stenosis (DORV with PS, SV with
In hypoplastic left heart syndrome, the only functional
PS). Biventricular surgical correction, when feasible,
ventricle RV acts as the main mixing and pumping
is most often limited by the adequacy of the PA size.
chamber. With a common pump, two resistance circuits
However, when single ventricle repair is planned, the
in parallel and flow returning to the same pump, this
is truly a parallel circulation. The output of the RV is pulmonary arteries should be of adequate size and the
distributed to the two circulations depending on the PA pressure should not exceed 15 to 20 mm and vascular
resistance of the two vascular beds (pulmonary and resistance should ideally be less than 2 wood units.m2
systemic). In a sick infant with hypoplastic left heart, and should not exceed 2 to 4 Wood units.m2.[15]
the systemic blood flow is markedly compromised with
postnatal reduction in PVR. A fine balance of PVR and EXAMPLES OF OXIMETRY STUDIES OF
SVR is to be maintained to ensure adequate systemic CYANOTIC HEART DISEASES
blood flow. In HLHS, it is best to keep the PBF equal to
SBF as well as keep the SBF near normal range so that the To simplify the discussion on systemic blood flow,
combined output of the ventricle will be twice normal. pulmonary blood flow and effective pulmonary (or
In admixture lesions, we discussed the normal arterio effective systemic) blood flow in various cyanotic heart
venous difference to be maintained at close to 25% to diseases, the following values are assumed:
maintain normal systemic blood flow. As the PA and An adult with body surface area, 1.6 m2 and assumed
aortic saturation are identical, aortic saturation 75% VO2, 200 ml/min; Hb, 14.75 gm%, with a cyanotic heart
usually ensures Qp/Qs close to unity (AO saturation – disease is the hypothetical patient.
systemic venous saturation/PV saturation-PA saturation).
However, this assumes PV saturation as 100% and SV VO2: 200 ml/min
saturation as 50%. Often, SV saturation will be very Hb: 14.75 gm%
low indicating poor tissue perfusion, even though the
AO saturation is 75%. Similarly, with increased PBF, O2 carrying capacity in ml/l of blood: 14.75 x 1.36 x 10
the systemic arterial saturation increases but may = 200 ml O2/l of blood
actually reduce the systemic blood flow due to steal Flow across vascular bed (l/min) = VO2/O2 carrying
by the pulmonary circulation, with tissue hypoxemia. capacity (ml O2/l of blood) x O2 saturation difference%
This steal often results in low diastolic pressure in the across vascular bed
AO, compromising coronary perfusion. This situation
can also cause rapid deterioration of hemodynamics. Flow (l/min) = 200/200 x O2 saturation difference%
This highlights the need for monitoring SV oxygen Flow (l/min) = 1/(O2 saturation difference%)
saturation along with arterial oxygen saturation. In the
first instance, the total cardiac output has to be increased Systemic blood flow [Qs] (l/min) = 1/(Aortic O 2
using positive inotropic agents, whereas in the second saturation% - PA O2 saturation%)
clinical scenario, PVR has to be increased usually using Pulmonary blood flow [Qp] (l/min) = 1/(PV O 2
controlled CO2 inhalation to cause mild hypercarbia saturation% - PA O2 saturation%)
or reducing inspired O2 concentration to cause mild
hypoxemia.[12] Effective pulmonary [Qep] or effective systemic [Qes]
blood flow = 1/(PV O2 saturation% – mixed venous O2
saturation%)
SURGERY IN CONGENITAL
CONGENITAL HEART DISEASE WITH To calculate the various flows, we need the oxygen
ADMIXTURE PHYSIOLOGY saturation in AO, PA, PV (often assumed as 100% or fully
saturated), and SV or mixed venous (MV) saturation
In patients with pulmonary hypertension and pulmonary (obtained as the average of three SVC and one IVC
vascular disease, the guidelines for surgery are generally saturation).
similar to an isolated VSD with pulmonary vascular
The following examples will have AO, PA, PV, and MV
disease: PVR index less than 4 Wood units.m2 having a
saturations, and with the VO2 and Hb% already given,
favorable outcome and those with PVR >8 Wood units.
we will proceed with calculation of the flows and
m2 having a poor outcome. Patients with PVRI dropping
interpretation.
to 6-8 wood units on 100% oxygen administered for 20
minutes and on nitric oxide are also offered surgical Please note that the O2 saturation difference between the
correction.[13] Patients with Qp : Qs ratio > 1.8 (PVR to AO and MV is kept at 20% to maintain normal systemic

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 Tharakan: Admixture lesions in CCHD

blood flow (cardiac output) and PV assumed as 100%, R  L shunt = 1.7 l/min and L  R shunt = 6.7 l/min
excluding any pulmonary cause for PV desaturation.
Discussion: The oximetry run reveals equal aortic and PA
Example 1 saturation typical of an admixture lesion. This is seen in
patients with TAPVC, common atrium, single ventricle,
and truncus arteriosus. The high saturation in the AO
at 90% indicates significantly increased pulmonary
blood flow (twice the systemic), as evident by the flow
calculations. Thus, the PVR is less than half of SVR. In
truncus arteriosus, this may indicate a favorable PVR for
surgical correction.

Example 3

MV 70%, AO 90%, PA 70%, PV 100%.

Calculated Qs = 5 l/min, Qp = 3.3 l/min, and Qep =

3.3 l/min

R L shunt = 1.7 l/min and L  R is Nil

Discussion: There is systemic desaturation, but the aortic

saturation is significantly more than the PA saturation.
This is the typical oximetry run of simple Tetralogy of
Fallot. There is no left to right shunt and only a right
MV 60%, AO 80%, PA 80%, PV 100%:
to left shunt. Thus, a simple TOF is not an admixture
lesion. However, TOF with AO to pulmonary shunt, Calculated Qs: 5 l/min, Qp; 5 l/min, Qep: 2.5 l/min
pulmonary atresia with VSD, and TOF with major AO to
R  L shunt 2.5 l/min and L  R shunt 2.5 l/min
PA collaterals will have bidirectional shunt. Among the
conditions which are grouped as TOF physiology with Discussion: The oximetry data show identical aortic
large VSD and subpulmonary obstruction (DORV with and PA saturations and hence is an admixture lesion.
PS, TGA with PS, single ventricle with PS, and corrected This can be seen in conditions like TAPVC, common
TGA with PS), only corrected TGA large VSD and severe atrium, truncus arteriosus, and single ventricle. The
PS will closely simulate the oximetry of TOF. aortic saturation is low and the pulmonary blood
flow is reduced. In conditions where PA pressures are
Example 2
expected to be at systemic levels as in truncus, single
ventricle (without PS), low aortic saturation suggests
pulmonary vascular disease and hence high surgical risk.
Pretricuspid admixture lesions like TAPVC in the absence
of obstruction and common atrium behave like large ASD
with progressive increase in pulmonary blood flow with
progressive reduction in RV hypertrophy and improved
RV compliance in infancy. In later age, if pulmonary
blood flow is reduced to the same level of systemic blood
flow, it is almost always due to increased PVR and RV
hypertrophy and reduced RV diastolic compliance. These
data would indicate poor surgical outcome because of
pulmonary vascular disease.

Examples 2 and 3 highlight the importance of systemic

arterial saturation, easily determined by pulse oximetry,
in assessing pulmonary blood flow and indirectly the
MV 70%, AO 90%, PA 90%, PV 100%:
pulmonary resistance. Clinical correlation is important
Calculated Qs: 5 l/min, Qp: 10 l/min, Qep: 3.3 l/min

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Tharakan: Admixture lesions in CCHD

to determine the site of increased pulmonary resistance: MV 60%, AO 80%, PA 90%, PV 100%.
at the peripheral vascular level (pulmonary vascular
Calculated Qs = 5 l/min, Qp = 10 l/min, Qep = 3.3 l/min.
disease) or proximally at valvular, supravalvular, or
subvalvular level (sub pulmonic stenosis). R  L shunt = 6.7 l/min and L  R shunt = 1.7 l/min.

Example 4 The oximetry data are of a patient with DORV and

subpulmonic VSD (Taussig Bing defect). Though DORV
is an admixture lesion, when the VSD is subpulmonic in
location, pulmonary venous return gets pumped into PA
from the LV resulting in unfavorable streaming. It results
in poor systemic saturation despite good pulmonary
blood flow.

Though the aortic saturation is low, the PVR will be lower

even when the PA systolic pressure equals the systemic
arterial systolic pressure because the pulmonary blood
flow in this patient is twice the systemic blood flow (PVR/
SVR ratio <= 0.5).

Examples 4 and 5 demonstrate the effect of favorable

streaming and unfavorable steaming on systemic arterial
saturation as well as the PVR. This often will call for
MV 70%, AO 90%, PA 80%, PV 100%. detailed hemodynamic study with pressures and flows
to assess PVR and surgical operability.
Calculated Qs: 5 l/min, Qp: 5 l/min, Qep, 3.3 l/min.
Example 6
R  L shunt = 1.7 l/min, L  R shunt = 1.7 l/min.

The oximetry data are of a patient with DORV and

subaortic VSD which is considered as an admixture lesion.
However, depending on the location of the VSD, favorable
or unfavorable streaming of oxygenated blood occurs in
patients with DORV. These data demonstrate favorable
streaming, with aortic saturation significantly higher
than PA saturation. However, the pulmonary blood flow is
just equal to the systemic blood flow. In DORV without PS,
the PA systolic pressure equals systemic systolic pressure
and hence this would indicate severe pulmonary vascular
disease despite a high aortic saturation. Note that despite
high systemic oxygen saturation, if favorable streaming
is present, pulmonary blood flow may be low and PVR
may be high in an admixture lesion.

Example 5

This discussion will not be complete without citing an

example of TGA. The O2 saturation in PA is far higher
than in the AO. Though it reflects the most unfavorable
streaming, the TGA anatomy with the great arteries arising
from the opposite ventricles facilitates all the pulmonary
venous return to reenter the PA (physiological left to right
shunt) and the SV return to AO (physiological right to left
shunt). The low Qep is the shunt across the atrial septal
defect which is bidirectional and necessary for survival.

CONCLUSION
CCHD with admixture physiology accounts for nearly 50%
of all cyanotic CHD. Proper assessment of hemodynamics

58 Annals of Pediatric Cardiology 2011 Vol 4 Issue 1

 Tharakan: Admixture lesions in CCHD

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Annals of Pediatric Cardiology 2011 Vol 4 Issue 1 59

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