Accepted: 22 January 2018

DOI: 10.1111/pan.13347

EDUCATIONAL REVIEW (COMMISSIONED)

Understanding cardiac shunts

Denise C. Joffe | Mark R. Shi | Carson C. Welker

Division of Pediatric Anesthesiology and

Pain Medicine, Department of
Anesthesiology and Pain Medicine,
University of Washington, Seattle, WA,
USA
Correspondence
Dr Denise C. Joffe, Department of
Anesthesiology and Pain Medicine, Seattle
Children’s Hospital, Seattle, WA, USA.
Email: denise.joffe@seattlechildrens.org
Section Editor: Mark Thomas
Summary
Most patients with congenital heart disease have a cardiac shunt whose direction
and magnitude can have a major impact on cardiorespiratory physiology and func-
tion. The dynamics of the shunt can be significantly altered by anesthetic manage-
ment and must be understood in order to provide optimal anesthetic care. Given
that there are now more adults than children with congenital heart disease and that
the majority of nonpediatric patients are cared for in centers without special exper-
tise in congenital heart disease, it is imperative that all anesthesia providers have a
general understanding of the subject. This educational review describes a technique
to explain this complex subject using simple pictorial diagrams.

KEYWORDS
cardiac, cardiac shunt, cath LAB, congenital heart disease, surgery

1 | INTRODUCTION 2 | PRINCIPLE OF MIXING

In a normal heart, blood courses in series from the right side to the
left side. Deoxygenated blood from the inferior vena cava (IVC),
superior vena cava (SVC) and a small amount of blood from the coro-
nary sinus (CS), all collectively referred to as the systemic venous
flow, is ejected out the pulmonary artery (PA) and is called the total
pulmonary blood flow (Qp). The same volume of blood returns oxy-
genated from the lungs and is ejected out the aorta. This is the total
systemic blood flow (Qs). The ratio of pulmonary to systemic blood
flow (Qp/Qs) is a fundamental relationship to understand in order to
appropriately manage patients with cardiac shunts. In patients with
normal hearts, pulmonary and systemic blood flows are equal, so Qp/
Qs is 1:1. However, Qp/Qs can become significantly altered in the
presence of a cardiac shunt. Anesthetic and surgical management can
have profound effects on shunt flow, which can lead to marked
changes in cardiac function. Therefore, understanding shunt physiol-
ogy is necessary for the delivery of optimal anesthetic care.
Pictorial diagrams are ideal teaching tools to help explain shunt
flow. Throughout this text, most of the figures depict the heart using
1 blood, which bypass the lungs through an intrapulmonary shunt, mix
squares and flows are represented by arrows (Figure 1). The length
of the arrow is proportional to the quantity of flow in liters per min-
ute (L/min) and the saturation is depicted by color: red indicates
oxygenated blood, blue indicates deoxygenated blood and purple is
an admixture. For the sake of simplicity, flows will be in familiar
adult numbers (ie, cardiac output of 5 L/min).
When blood with different saturations or oxygen contents is mixed
together, the resultant saturation or oxygen content is proportional
to the volume and saturation, or volume and oxygen content, of
the blood in the mixture. For example, when 2 equal volumes of
blood with a saturation of 100% and 60% are mixed together, the
resultant saturation is 0.5 9 100% + 0.5 9 60% = 80%, where 0.5
is the proportion of each volume. Alternatively, the final saturation
of a mixture of blood with 20% of the volume at a saturation of
100% and 80% of the volume with a saturation of 60% is
0.2 9 100% + 0.8 9 60% or 68%. Finally, if venous return from
the IVC is 65% of the total flow into the RA and has a saturation
of 78%, while SVC flow is 30% with a saturation of 77%, and the
CS is 5% of flow with a saturation of 25%, the net saturation
entering the PA is 0.65 9 78% + 0.30 9 77% + 0.05 9 25% =
75% (Figures 2A-B).
The net oxygen content of a mixture of blood with varying con-
tents is illustrated using the lungs as an example in which oxy-
genated blood exiting the pulmonary capillaries and deoxygenated
to enter the left atrium (LA) as arterial blood. The net oxygen con-
tent is the sum of the oxygen content from the capillaries (ie, about
95% or 0.95 of total flow) and the fraction from intrapulmonary
shunt (ie, about 5% or 0.05 of total flow). Therefore, the resultant
oxygen content of arterial blood (QtotalCaO2) is:

Pediatric Anesthesia. 2018;1–10. wileyonlinelibrary.com/journal/pan © 2018 John Wiley & Sons Ltd | 1
2 | JOFFE ET AL.

(A)

(B)

F I G U R E 1 Schematic representation of a normal heart with

arrow orientation showing the direction of flow, size representing
magnitude of flow, and color indicating the saturation of blood in
each chamber. Note that Qp = Qs in a normal heart and Qp and Qs
arrow sizes are equal. QsSVC = superior vena cava systemic venous
flow, QsIVC = inferior vena cava systemic venous flow,
QsCS = coronary sinus flow, Qp = total pulmonary blood flow,
Qs = total systemic blood flow, and Qpv = pulmonary venous flow.
Chambers and major vessels are labeled RA = right atrium,
RV = right ventricle, LA = left atrium, LV = left ventricle,
PA = pulmonary artery and Ao = aorta

F I G U R E 2 A, The resulting saturation of a mixture of blood in

QtotalCaO2 ¼ foxygenated lung flowg þ shunt flow
QtotalCaO2 ¼ ½ðQtotal - QshuntÞ  CcO2  þ ½Qshunt  CvO2 
QtotalCaO2 ¼ 0:95  20:5 þ 0:05  15 ¼ 20:2 mL O2 =dL
where C is oxygen content, c is capillary blood, v is mixed venous
blood, a is arterial blood, Qtotal-Qshunt is flow going to
oxygenated lung and Qshunt is the intrapulmonary shunt flow
(Figure 3).
However, this calculation cannot be applied to determine the
which 20% has a saturation of 100% and 80% has a saturation of
68%. B, The PA saturation is a combination of the QSSVC, QSIVC,
and QSCS flows. In this example, the proportion of total systemic
venous blood flow from each vessel must be calculated.
QSIVC = 3.25 L/min  5 L/min = 0.65, QSSVC = 1.5 L/min  5 L/
min = 0.3, QSCS = 0.25 L/min  5 L/min = 0.05. The proportion of
flow from each vessel is then multiplied by its respective saturation
to determine the final PA saturation:
0.65 9 78% + 0.3 9 77% + 0.05 9 25% = 75%
(Qshunt), which is deoxygenated blood that bypasses alveoli and

partial pressure of oxygen (PO2) in a mixture of blood with different does not undergo gas exchange, to total pulmonary blood flow (Qto-

partial pressures because there is a nonlinear relationship between tal). The ratio is a measure of lung disease and has no link to cardiac

oxygen saturation and PO2 due to the sigmoid nature of the oxy- shunts or congenital heart disease (CHD). It is confusing that very

hemoglobin dissociation curve. For example, at the top of the curve, similar subscripts are used for entirely different concepts.

once the saturation of blood reaches 100%, PaO2 can vary widely.
Therefore, the PaO2 of equal volumes of blood with PaO2 of
400 mm Hg and a PaO2 of 500 mm Hg is not 450 mm Hg and can-
not be determined without direct measurement.
3 | Qs/Qt VERSUS Qp/Qs
It is important to differentiate Qs/Qt that we just discussed from
Qp/Qs to be explained below. Qs/Qt is the short hand designation
for intrapulmonary shunt fraction; the ratio of pulmonary shunt flow
4 | DETERMINING IF THERE IS A SHUNT
It is helpful to think of an impervious wall separating the right and
left sides of a normal heart. Blood entering the PA cannot be more
oxygenated than the weighted sum of the contributions from the
SVC, IVC and CS without implicating a left-to-right shunt (Figure 4).
The shunt can be intracardiac, that is, from an atrial septal defect
(ASD), ventricular septal defect (VSD), or atrioventricular canal defect
(AVC). A shunt can also be extracardiac, such as a patent ductus
JOFFE ET AL.
F I G U R E 3 A schematic utilizing another application of the theory
of mixing using the oxygen content from oxygenated and shunted
lung segments in the lungs (rather than saturations) to determine the
oxygen content in arterial blood
arteriosus (PDA), aortopulmonary collaterals, an aortopulmonary win-
dow, or a ruptured sinus of valvsalva aneurysm in which blood that
has exited the heart then shunts from the aorta to either the pul-
monary artery, right atrium, or right ventricle.
Likewise, the saturation of blood in the aorta is a combination of
the saturation in each pulmonary vein multiplied by the proportion of
flow through each vein. If the aortic saturation is any lower, then a
right-to-left cardiac shunt is present (Figure 5). Examples of right-to-
left intracardiac shunts include unrepaired Tetralogy of Fallot (Fig-
ure 5A) and patients with a Glenn procedure (ie, cavopulmonary anas-
tomosis, Figure 5B). Extracardiac right-to-left shunts can be the result
F I G U R E 4 A VSD is an example of a simple left-to-right shunt.
The magnitude of the shunt: QpQs (6 L/min5 L/min = 1 L/min)
returns to the pulmonary circulation through the VSD so that the PA
saturation is higher than systemic venous saturation. Qp > Qs.
Systemic venous return (Qs IVC/SVC/CS) has been consolidated in
this and the following figures for simplicity
| 3
of systemic venous collaterals draining to the pulmonary veins or left
atrium, or shunting from the PA to the aorta in patients with a PDA
and pulmonary hypertension (PHTN). Of course, if pulmonary venous
blood is desaturated because of lung disease, then the aortic satura-
tion would be low without invoking the presence of a cardiac shunt.
The shunt is “simple” if it is an isolated left-to-right or right-to-
left shunt. Patients with a bidirectional shunt have both a left-to-
right and right-to-left shunt. The shunts are usually not equal with
the left-to-right component often larger since PVR is lower than
SVR leading to greater pulmonary blood flow. In patients with a bidi-
rectional shunt, the PA saturation is higher than the saturation of
systemic venous blood and the aortic saturation is less than pul-
monary venous blood. It is noteworthy that most patients with com-
plex CHD such as unrepaired single ventricle (SV) physiology,
transposition of the great arteries (TGA), and truncus arteriosus have
bidirectional shunts (Figures 6A-C).
5 | CALCULATING Qp/Qs AND
RECIRCULATED FLOW IN PATIENTS WITH
SIMPLE SHUNTS
The presence, size, and direction of a shunt are usually measured in
the cardiac catheterization (cath) laboratory but the ratio can be cal-
culated in the operating room (OR) when there is concern about the
size of a residual shunt after repair. Echocardiography using color
flow and spectral Doppler can usually identify the direction of a
shunt and occasionally provide a rough estimate of Qp and Qs
although it is not very accurate and not used for precise quantifica-
tion.
6 | CALCULATING Qp/Qs IN THE CATH
LABORATORY
In the cath laboratory, Qp and Qs are measured separately and the
ratio is then calculated. While thermodilution is often used to calcu-
late cardiac output, it is not an accurate method of measurement in
patients with cardiac shunts for 2 main reasons. First, thermodilution
measures Qp and then assumes Qs is equal, which is not true in the
presence of a cardiac shunt. Second, recirculation of cold contrast to
the right heart through an ASD or VSD for example, causes an
underestimation of flow.2
Therefore, Qp and Qs must be measured individually using the
appropriate Fick equation:
Qs ¼ VO2 ðconsumptionÞ=½CaO2  CvO2 
Qp ¼ VO2 ðuptakeÞ=½CpvO2  CpaO2 
where CaO2 is arterial oxygen content, CvO2 is systemic venous
oxygen content, CpvO2 is pulmonary venous oxygen content, and
CpaO2 is pulmonary artery oxygen content. VO2 is total body oxy-
gen consumption, which is also equal to VO2 uptake by the lungs
4 |
(A)
(B)
F I G U R E 5 A, Tetralogy of Fallot is an example of a simple right-to-
left shunt. The magnitude of the shunt is QsQp (5 L/min2 L/
min = 3 L/min) of systemic venous flow that is shunted right-to-left
through the VSD. The arterial saturation is lower than the PV
saturation. Qp < Qs. B, A schematic diagram of a heart with a Glenn
anastomosis (cavopulmonary anastomosis). The SVC is anastomosed
directly to the PA. Deoxygenated blood from IVC flow enters the RA
and mixes with oxygenated blood from pulmonary venous return via
the Glenn. Note that the PA saturation is the same as the SVC
saturation, but the aortic saturation is purple and it should be red.
Therefore, this is a simple right-to-left shunt. The magnitude of the
shunt is QsQp (5 L/min2.5 L/min = 2.5 L/min). These are examples
of cyanotic lesions with decreased pulmonary blood flow (PBF)
since we do not “store oxygen.” VO2 uptake and VO2 consumption
are related to metabolic rate and can be estimated based on values
taken from an oxygen consumption table.
Oxygen content (CaO2) is calculated by adding the quantity of
oxygen carried by hemoglobin and a smaller quantity of dissolved
oxygen. This equation is used to calculate oxygen content in each cir-
culation (arterial, venous, pulmonary artery, and pulmonary venous)
by using the appropriate saturation and partial pressure of oxygen.
JOFFE ET AL.
{carried} + {dissolved}
fcarriedg þ fdissolvedg
CaO2 ¼ Hgb (g/dL)  1:34 mL O2 =Hgb (g)  SpO2ð%Þ
þ PO2 ðmm HgÞ  0:003 ðmL O2 =mm Hg=dLÞ
The inspired oxygen is usually decreased to room air (ie,
FiO2 = 0.21), so that, PaO2 is not appreciable and the dissolved oxy-
gen content portion can be ignored. Therefore,
CaO2 ¼ Hgb ðg/dLÞ  1:34 mL O2 =Hgb (g)  SaO2ð%Þ
Samples are taken from the aorta, SVC, and PA and the oxy-
gen content of each is calculated by substituting the appropriate
saturation. Usually, a pulmonary venous saturation is not measured
directly unless there is suspicion that there is a pathologic intra-
pulmonary shunt because the sample is often difficult to obtain.
Therefore, a small “physiologic” intrapulmonary shunt is presumed
and a pulmonary venous saturation of 96% or the patient’s sys-
temic saturation (if higher than 96%) is used to calculate oxygen
content of pulmonary venous blood. Note that in the presence of
an extracardiac left-to-right shunt from the aorta to the pulmonary
artery (eg, a PDA), obtaining an accurate PA sample may
be impossible because the shunt often enters the distal main
or left PA and there is inadequate mixing for a reliable measure-
ment.
Once oxygen content is known, Qp and Qs can be calculated
from the Fick equation and Qp/Qs can be determined.
7 | CALCULATING Qp/Qs IN THE OR
In the OR, a “short cut” version of Qp/Qs can be calculated without
actually measuring Qp or Qs by using a simple algebraic manipula-
tion of the equation and factoring out common components.
Qp/Qs ¼ ½VO2 ðuptakeÞ=½CpvO2  CpaO2 =½VO2 ðconsumptionÞ=
½CaO2  CvO2 
Qp/Qs ¼ ½CaO2  CvO2 =½CpvO2  CpaO2 
As previously mentioned, total body oxygen consumption equals
uptake, so VO2 (uptake) and VO2 (consumption) cancel out, while
Hg 9 1.34 are factored out and cancel each other, and dissolved
oxygen is ignored if the patient is on minimal supplemental oxygen.
This simplifies Qp/Qs to the following,
Qp/Qs ¼ ½SaO2  SvO2 =½SpvO2  SpaO2 
Blood from the SVC and PA is obtained by the surgeon by directly
sampling the vessel. Alternatively, if a PA catheter or PA line is pre-
sent, the anesthesiologist can obtain samples from the PA as well as
the side port of the introducer (not the proximal port of the PA cathe-
ter which is in the RA) to get an SVC saturation. Samples must be
JOFFE ET AL. | 5

A B C

F I G U R E 6 Three examples of common CHD lesions with bidirectional shunts and excessive PBF. A, A schematic diagram of single ventricle
physiology with 1 atrium and 1 ventricle and 2 unobstructed great vessels. After the first hours of life, the PVR drops, so that more flow goes
to the lungs than out the aorta. Note that the PA saturation is higher than it should be and the aortic saturation is lower than it should be
therefore, this is a complex bidirectional shunt. B, TGA. The PA saturation is higher than the SVC and IVC saturation and the aortic saturation
is lower than the pulmonary venous saturation, therefore a bidirectional shunt is present. C, Truncus arteriosus. The PAs and aorta originate
from a common root. The PA saturation is higher than it should be and the aortic saturation is lower than it should be

obtained proximal to the location of the suspected shunt, so an RA
saturation is not an appropriate substitute for an SVC sample. Usually,
the pulse oximeter is adequate to estimate aortic and pulmonary
venous saturation unless a right-to-left shunt is suspected in which
case the pulmonary venous saturation is assumed to be “normal”
(96%) as described above. To reiterate, the pulmonary venous satura-
tion is not assumed to be abnormally low unless there is a suspicion
for lung disease. Therefore, in the case of a right-to-left shunt, the pul-
monary venous saturation is assumed to be normal (96%) and arterial
desaturation is the result of systemic venous blood crossing to the
arterial circulation. It is crucial to include the dissolved quantity of oxy-
gen in the calculation (ie, PO2 9 0.003) if the patient is on more than
50% oxygen, so that a partial pressure of oxygen 9 0.003 from each
vessel must be included in the calculation.
A Qp/Qs ratio greater than 1.5-2:1 is considered a clinically sig-
nificant left-to-right shunt that warrants consideration to close or
return to bypass and reattempt closure. A value less than 1 implies a
right-to-left shunt is present.
Once Qp and Qs are known, shunt flow which is also referred to
as the recirculated flow, is calculated by subtracting Qp from Qs
(right-to-left shunt) or Qs from Qp (left-to right shunt) (see Fig-
ures 4-5). Note that the absolute quantity of shunt flow cannot be
determined if the shorthand method is used to calculate Qp/Qs
since Qp and Qs are never measured.
8 | RESTRICTIVE VERSUS UNRESTRICTIVE
SHUNTS
Small shunts are termed restrictive and imply that the amount of flow
through the shunt is limited by the small size of the defect. By defini-
tion, there is a large pressure difference between the chambers
connected via the shunt. Unrestrictive shunts are large and the quan-
tity of flow through the shunt can vary with changes in hemodynamic
conditions. For example, the direction of flow through an unrestrictive
VSD largely depends on the balance between SVR and PVR. Further,
the pressure gradient between the 2 connected chambers is minimal.
9 | CALCULATING Qp/Qs, SHUNT FLOWS
AND EFFECTIVE FLOWS IN PATIENTS WITH
A BIDIRECTIONAL SHUNT
In the presence of a bidirectional shunt, there is shunting of blood
from the systemic venous circulation to the systemic arterial circula-
tion and from the pulmonary venous circulation to the pulmonary
arterial circulation. In essence, there is deoxygenated blood that
recirculates to the aorta and oxygenated blood that goes back to the
lungs. The Qp and Qs are determined using the Fick equation as
described above, however, calculating the recirculated flow (ie, the
shunt) requires understanding a new concept and learning a new
equation.
Effective blood flow is the component of the total flow out of
each great vessel that comes from the physiologically appropriate
circulation (Figure 7). In other words, effective pulmonary blood flow
(PBF) is the component of Qp from the systemic venous circulation
(deoxygenated blood that is available to carry oxygen) and effective
systemic blood flow (SBF) is the fraction of Qs from the pulmonary
venous circulation (oxygenated blood that delivers oxygen). In con-
trast, recirculated PBF is that component of Qp from the pulmonary
veins (oxygenated blood returning to the lungs) and recirculated SBF
is that part of Qs from the SVC and IVC (deoxygenated blood
returning to the body). Total flows (ie, Qp and Qs) equal the sum of
the recirculated and effective blood flows.
6 |
Qp ¼ Qeff PBF þ Qrecirc PBF
Qs ¼ Qeff SBF þ Qrecirc SBF
In a normal heart, Qp = Qs = effective flow and recirculated flow
is zero. However, in patients with cardiac shunts, Qs and Qp are not
always equal and recirculated flows can also vary from zero (no
shunt) to greater. It is extremely important to understand that effec-
tive flows are always equal, otherwise one side of the circulation
would become depleted. Effective PBF is determined using the fol-
lowing equation:
Qeff PBF ¼ VO2 ðuptakeÞ=½CpvO2  CvO2 
where CvO2 is systemic venous oxygen content and CpvO2 is pul-
monary venous oxygen content.
The equation essentially measures the proportion of systemic
venous blood (as represented by CvO2) that gets oxygenated
(CpvO2). Once Qeff PBF is calculated, then Qeff SBF is known since
they are equal. Shunt flow can then easily be determined by sub-
tracting effective flow from total flow.
10 | SHUNTING IN TRANSPOSITION OF
THE GREAT ARTERIES (TGA)
The physiology of blood flow in TGA is unique among CHD lesions
and new nomenclature is necessary to describe the circulation (Fig-
ure 8). Anatomic shunt describes the flow from either the right heart
(including the aorta) or flow from the left heart (including the PA) to
the opposite circulation. In other words, the anatomic right-to-left
F I G U R E 7 This diagram is identical to Figure 6A but breaks
down the components of total flow through each great vessel. Total
pulmonary blood flow (Qp) is composed of effective PBF and
recirculated PBF. Total systemic blood flow is composed of effective
SBF and recirculated SBF. Note that effective flows are always
equal, whereas recirculated flows and total flows may not be. The
ideal scenario is a balanced circulation and occurs when Qp ffi Qs. In
that case, the recirculated flows and the total volume work of the
ventricle is the least and oxygen delivery is optimal. Assuming a
pulmonary venous saturation of 96% and a systemic venous
saturation of 60%, the arterial saturation would be
(0.5 9 96) + (0.5 9 60%) = 78%
JOFFE ET AL.
shunt is flow from the RA to the LA through the ASD or from the
aorta to the PA through the PDA, and the anatomic left-to-right
shunt is the flow from the left atrium (LA) to the right atrium (RA)
through the ASD. Therefore, in TGA, blood that shunts to the oppo-
site circulation is actually the effective blood flow as described in the
previous section. As in all hearts, the total flow out each great vessel
is composed of effective flow and recirculated flow and each is cal-
culated using the Fick equation in a similar manner to normally
related great vessels. Qs is calculated using aortic and mixed venous
saturation and Qp using pulmonary artery and pulmonary venous
saturation even though the vessels are in the incorrect position. Qp
is much greater than Qs in TGA because PVR is significantly less
than SVR, although the fraction of both Qp and Qs that is recircu-
lated flow is much larger than the effective flow (Figure 8). This
physiology is unique to TGA because despite the significantly
increased Qp/Qs that is often greater than 2:1, the volume of PBF
does not dictate the oxygen saturation like in other cardiac lesions
because most of the pulmonary flow simply recirculates back to the
lungs. Only the much smaller component of oxygenated pulmonary
venous blood that shunts across the ASD to the right heart and
aorta provides oxygen for consumption since most of the aortic
blood flow is also recirculated deoxygenated blood.
11 | CHAMBER ENLARGEMENT IN
PATIENTS WITH SHUNTS
Chamber enlargement occurs as a result of excess volume loads
imposed on the heart. In these diagrams, chambers with longer
arrows have higher flow rates and hence can become pathologically
enlarged as they remodel. However, patients with VSDs are excep-
tions to this logic because there is only left heart dilation without
any effect on the RV size despite the left-to-right shunt, which
would be expected to increase RV volume (see Figure 4). This can
be explained because VSD flow occurs predominantly during systole
when the pulmonary valve is open. Therefore, the RV does not incur
the burden of ejecting the increased volume load since the LV effec-
tively does all the volume work and the RV only serves as a conduit.
The increased blood flow then returns to the LA causing enlarge-
ment of left sided chambers. Over time, patients with a VSD may
develop PHTN leading to right-sided chamber enlargement but this a
late sequela.
Using hypoplastic left heart syndrome (HLHS) as an example of a
single ventricle (SV) lesion, these diagrams can help illustrate why a
Glenn procedure performed in patients with SV physiology markedly
decreases the volume load on the ventricle despite similar arterial
saturations. The first step of a staged palliation for SV physiology is
the Norwood procedure, after which the single ventricle ejects SVC,
IVC, and pulmonary venous blood into both the systemic and pul-
monary circulations via a Blalock Taussig (aortopulmonary connec-
tion) or Sano shunt (RV to PA connection) (Figure 9). The second
stage is a Glenn procedure, after which the SV ejects IVC flow and
pulmonary venous flow (which originates as SVC flow from the
JOFFE ET AL.
F I G U R E 8 In TGA, the majority of deoxygenated systemic
venous blood recirculates to the aorta and the majority of
oxygenated pulmonary venous blood recirculates to the lungs. There
is a small amount of blood crossing through the ASD that would be
considered “the shunt” in other lesions but provides the effective
blood flow in TGA. The effective systemic blood flow is the
component of total systemic flow that originates from the lungs and
provides the oxygen for the body’s consumption. The effective
pulmonary blood flow is the component of total pulmonary blood
flow that originates from the systemic venous circulation. The blood
is deoxygenated and available to carry oxygen
Glenn) resulting in a significantly decreased volume load of 5 L/min
vs 10 L/min on the SV. (see Figure 5B).
12 | CLINICAL IMPLICATIONS OF AN
ABNORMAL Qp/Qs RATIO
As discussed previously, an abnormal Qp/Qs ratio suggests the pres-
ence of a cardiac shunt. In a simple right-to-left shunt, Qp/Qs is less
than one. Since deoxygenated blood bypasses the pulmonary circula-
tion, the resulting hypoxemia is unresponsive to supplemental oxy-
gen. The degree of cyanosis depends on the magnitude of the right-
to-left shunt, which can vary based on the underlying pathophysiol-
ogy. In general, arterial saturations above 75% are tolerated although
exercise capacity may be limited when saturations are chronically in
the lower 70s. When saturations are consistently lower than 70-
75%, treatment is warranted. Therapy depends on the lesion: In
patients with TOF, complete repair, palliation with a Blalock-Taussig
shunt (subclavian artery to pulmonary artery) or less commonly med-
ical treatment such as beta blockers can be offered. In patients with
a Glenn, performing a Fontan procedure, which directs IVC blood to
the pulmonary artery, so that all systemic venous blood (except for
the coronary sinus) enters the pulmonary circulation, is often an
option. Occasionally, lung disease or systemic venous to left heart
| 7
F I G U R E 9 Schematic of a patient with HLHS and a Sano shunt.
Compare the total volume work performed by the single ventricle
(10 L/min) to Figure 5B after a Glenn procedure is performed (5 L/min)
collaterals can be treated. Chronic hypoxemia can result in erythro-
cytosis, elevated blood viscosity and increased risk of thrombotic
stroke. In addition, significant hypoxia can compromise neurologic
development and cause myocardial, renal, and hepatic dysfunction.
Alternatively, a simple left-to-right shunt will result in Qp/Qs
greater than one. Patients have normal arterial saturations and ini-
tially they are often asymptomatic. However, chronic pulmonary
overcirculation leads to congestive heart failure, myocardial dysfunc-
tion and less commonly systemic hypoperfusion. The most lethal
complication is the development of pulmonary vascular disease (eg,
PHTN) leading to right heart failure and eventual shunt reversal
(Eisenmenger’s physiology).
Many patients with unrepaired complex CHD and bidirectional
shunts, are cyanotic yet often have pulmonary overcirculation and
significantly elevated Qp/Qs. This is due to decreased pulmonary
vascular resistance (PVR) relative to systemic vascular resistance
(SVR) that preferentially favors excess PBF (see Figures 6 and 7).
Patients with SV anatomy often have left or right ventricular outflow
tract obstruction and require ductal patency for survival. Therefore,
the systemic and pulmonary circulations are interdependent even
with obstruction of a great vessel. The most common symptoms in
unrepaired patients are pulmonary edema, congestive heart failure,
and cyanosis. Congestive symptoms usually develop within the first
few days of life as PVR decreases. The systemic saturation concomi-
tantly increases into the high 80-90’s as the fraction of Qs made up
of recirculated pulmonary venous blood increases (see Figure 7). In
8 |
fact, a lack of symptoms in these patients is concerning for persis-
tently elevated PVR. In some cases, pulmonary overcirculation is so
severe, that systemic perfusion is compromised. However, for the
majority of patients with unrepaired complex CHD, symptoms of
pulmonary overcirculation are an indication for surgery in order to
avoid further decompensation.
13 | ANESTHETIC MANAGEMENT OF
PATIENTS WITH CARDIAC SHUNTS
Most patients with known cardiac shunts do not have a cath or a
measured Qp/Qs. However, understanding the anatomy and physiol-
ogy of their lesion enables the anesthesiologist to predict the ratio
of Qp/Qs and anticipate the changes that the anesthetic will have
on hemodynamics.3 As described above, there are few lesions with
Qp/Qs < 1 such as TOF or patients with a Glenn. Saturations below
70-75% in the absence of lung disease indicate decreased Qp/Qs
that is usually less than 0.5 to 1. Simple lesions with left-to-right
shunting such as ASD, VSD, PDA, and atrioventricular canals will
have Qp/Qs >1. The severity of congestive heart failure and the
degree of chamber dilation usually indicates the Qp/Qs is signifi-
cantly elevated. Most complex lesions have bidirectional shunts. In
those cases, the ideal physiology is present when Qp ffi Qs resulting
in tolerable saturations (75%), avoidance of pulmonary overcircula-
tion, and a minimum extra volume work imposed on the SV (see Fig-
ure 7). A saturation that deviates significantly from 75%-80% can
provide a rough estimate of the Qp/Qs ratio in most cases. An
important exception is the unique physiology of TGA in which the
magnitude of the elevated Qp/Qs cannot be predicted by arterial
saturation.
In patients with restrictive shunts, there are minimal clinical
implications or consequences for anesthesia management beyond
the need for vigilance to avoid air in iv lines or an appreciation that
cardiac output measured with a pulmonary artery catheter will be
inaccurate. In contrast, in patients with nonrestrictive defects, shunt
flow largely depends on the balance between SVR and PVR and they
can be significantly affected by anesthetic technique. In the case of
left-to-right shunts, either decreases in PVR and/or increases in SVR
can increase Qp. Induction of anesthesia is particularly precarious
because hyperventilation is common when patients are paralyzed
and ventilation is assumed by the anesthesiologist. In addition,
increases in SVR as a result of stress, pain, and light anesthesia add
to increases in the left-to-right component of shunt flow. The
increase in Qp is especially dangerous in patients with lesions such
as truncus arteriosus, HLHS and aortopulmonary window because
retrograde flow from the aorta into the PA during diastole can be so
large that it results in lower aortic diastolic blood pressures and
myocardial ischemia. In order to reduce decreases in PVR, it is crucial
to minimize FiO2 and avoid hyperventilation. Increases in SVR can
be reduced by ensuring adequate analgesia and anesthetic depth
especially during airway manipulation. Another vulnerable time for
patients with either a simple left-to-right shunt or a bidirectional
JOFFE ET AL.
shunt with a large left-to-right component, occurs during cardiac sur-
gery after sternotomy when the lungs expand and intrathoracic pres-
sure drops, causing a further decrease in PVR. The increased shunt
can compromise systemic perfusion. If hemodynamic instability
ensues, the surgeon can place tourniquets around the PAs and tem-
porarily restrict flow into the lungs in an attempt to “re-balance” the
circulation.
The direction of flow through an unrestrictive ASD is more com-
plicated since it depends on differences in ventricular compliance
which in turn is related to multiple factors such as heart rate, ven-
tricular wall thickness, preload, and afterload. Anesthetic manage-
ment rarely results in significant changes in the direction or quantity
of flow through the ASD.
In patients with simple right-to-left shunts, the degree of shunt-
ing depends on the etiology of the shunt. In patients with TOF, the
shunt is mostly the result of dynamic subpulmonary obstruction that
can worsen with increases in sympathetic tone, tachycardia,
increases in contractility and hypovolemia and result in a cyanotic
“tet spell.” The treatment should address the precipitating factor and
commonly involves the administration of a combination of volume,
vasopressors, beta blockers, and opioids.
In patients with Glenn physiology, an acute decrease in the arte-
rial saturation can be the result of a drop in SVC flow (with a con-
comitant increase in IVC flow), a decrease in the pulmonary venous
saturation or a decrease in SVC or IVC saturations (see Figure 5B).
Decreases in SVC flow can be a result of aggressive use of positive
pressure ventilation. SVC flow can also be altered by changes in
PaCO2 independent of changes in ventilation pressure because cere-
bral blood flow is exquisitely sensitive to PaCO2.4 Maintaining the
PaCO2 in the mid 40s can help increase internal jugular flow and
therefore Glenn flow, and improve oxygenation. Paradoxically, the
benefit of a higher PaCO2 on increasing Qp usually outweighs any
increase in PVR caused by PaCO2-induced respiratory acidosis. Fig-
ure 5B illustrates why it is necessary to optimize pulmonary venous
and systemic venous saturation since they combine to make up Qs.
Increasing pulmonary venous saturation may require administration
of oxygen to treat pulmonary disease. Increasing systemic venous
saturation may require inotropes or red blood cell transfusion to
improve oxygen delivery.
In patients with PHTN and a PDA, increases in PVR will wor-
sen the right-to-left shunt. Therefore, techniques to decrease PVR
(and possibly increase SVR) are warranted. Increasing the FiO2,
slight hyperventilation, decreases in airway pressure, medical ther-
apy with nitric oxide and inodilators such as milrinone will all help
decrease PVR. Treatment of stress, pain, and hypothermia are also
options.
The speed of induction varies with the mode of induction (ie,
intravenous or inhalational) and the direction of the shunt. Right-to-
left shunts result in a more rapid intravenous induction as the intra-
venous agent travels in blood that bypasses the lungs and enters the
systemic circulation where it is more quickly distributed to its site of
action. In contrast, an inhalational induction in a patient with right-
to-left shunting is slowed as shunted blood, which contains no
JOFFE ET AL.
anesthetic, dilutes the partial pressure of anesthetic gas in blood that
underwent gas exchange. This effect is most profound for poorly
soluble anesthetics, where the dilution effect is greatest. Left-to-
right shunting has little effect on either IV or inhalational inductions.
The presence of any cardiac shunt, no matter the directionality,
makes de-airing intravenous fluids essential to avoiding the potential
for iatrogenic air embolism.
14 | SUMMARY
1. Diagrams illustrating the magnitude, direction, and saturation of
flow in the presence of cardiac shunts can help assist the anes-
thesiologist with proper understanding and management of com-
plex congenital heart diseases.
2. The ratio of Qp/Qs for simple shunts can be calculated quickly in
the operating room in a patient with a pulmonary artery catheter
or during open cardiac surgery from the ratio of their respective
simplified Fick equations: Qp/Qs = [SaO2  SvO2]/
[SpvO2  SpaO2].
3. A simple left-to-right shunt is present when the PA saturation is
greater than the systemic venous saturation and Qp/Qs > 1. A
simple right-to-left shunt is present when the aortic saturation is
less than the pulmonary venous saturation and Qp/Qs < 1. A
complex bidirectional shunt is present when both a left-to-right
and right-to-left shunt is present, so that the PA saturation is
greater than the systemic venous saturation and aortic saturation
is less than the pulmonary venous saturation. Most patients with
bidirectional shunts have a Qp/Qs > 1, in other words the left-
to-right component of the shunt predominates. They are cyanotic
and have pulmonary overcirculation.
4. To calculate the left-to-right and right-to-left components of
shunt present in patients with complex bidirectional shunts,
effective pulmonary blood flow must first be determined (Qeff
PBF = VO2 (uptake)/[CpvO2  CvO2]). Once Qeff PBF is deter-
mined, then Qeff SBF is known because they are always equal.
Qrecirc PBF and SBF can then be calculated as the difference
between Qp and Qeff PBF and Qs and Qeff SBF, respectively.
5. Transposition physiology is unique because the blood that
crosses to the opposite circulation is the effective flow and not
the shunt. In addition, the volume of PBF does not dictate the
oxygen saturation like in other cardiac lesions; the degree of
intercirculatory mixing does, meaning the quantity of effective
systemic blood flow.
6. Physiologic sequelae of right-to-left shunting include cyanosis, ery-
throcytosis, increased risk of thrombotic stroke and end organ dys-
function due to poor O2 delivery. Physiologic sequelae of left-to-
right shunting include chamber enlargement and pulmonary over-
circulation resulting in pulmonary edema, poor gas exchange, and
in some cases irreversible increases in PVR. Clinical manifestations
of unrepaired complex bidirectional shunts will have some element
of both depending on the underlying physiology.
| 9
7. Proper anesthetic management of patients with CHD depends on
the underlying lesion and an understanding of how induction,
maintenance, and emergence from anesthesia influence their
unique physiology.
15 | REFLECTIVE QUESTIONS
1. Which of the following is an example of a bidirectional shunt?
a. SaO2 85%, SvO2 65%, SpvO2 98%, SpaO2 65%
b. SaO2 100%, SvO2 75%, SpvO2 100%, SpaO2 75%
c. SaO2 85%, SvO2 65%, SpvO2 98%, SpaO2 75%
d. SaO2 89%, SvO2 65%, SpvO2 89%, SpaO2 65%
e. SaO2 98%, SvO2 65%, SpvO2 98%, SpaO2 80%
Answer: C
In a complex bidirectional shunt, the PA oxygen saturation is
higher than systemic venous saturation and Ao oxygen saturation is
lower than pulmonary venous saturation. Answer C is the only
appropriate choice because both SaO2 < SpvO2 and SpaO2 > SvO2
are true.
2. Which of the following patients is likely to benefit from oxygen
therapy?
a. SaO2 85%, SvO2 65%, SpvO2 98%, SpaO2 65%
b. SaO2 100%, SvO2 75%, SpvO2 100%, SpaO2 75%
c. SaO2 85%, SvO2 65%, SpvO2 98%, SpaO2 75%
d. SaO2 89%, SvO2 65%, SpvO2 89%, SpaO2 65%
e. SaO2 98%, SvO2 65%, SpvO2 98%, SpaO2 80%
Answer: D
In answer D, Ao saturation is equal to pulmonary venous satura-
tion, albeit both lower than would be expected of oxygenated blood
returning from the lungs. PA saturation is equal to systemic venous
saturation. Because of this, no cardiac shunt is present. Instead,
these values suggest the presence of an intrapulmonary shunt or V/
Q mismatch, which is more likely to respond to supplemental O2
than the remaining answer choices where cyanosis is present
(Answers A and C) as they are secondary to right-to-left shunting.
Oxygen therapy administered to a patient with a left-to-right shunt
will increase the shunt resulting in worsening pulmonary overcircula-
tion and should not affect the saturation unless it results in worsen-
ing pulmonary edema.
3. Calculate Qp/Qs for each of the following:
a. SaO2 85%, SvO2 65%, SpvO2 98%, SpaO2 65%
b. SaO2 100%, SvO2 75%, SpvO2 100%, SpaO2 75%
c. SaO2 85%, SvO2 65%, SpvO2 98%, SpaO2 75%
d. SaO2 89%, SvO2 65%, SpvO2 89%, SpaO2 65%
10 | JOFFE
e. SaO2 98%, SvO2 65%, SpvO2 98%, SpaO2 80%
Answer: Using the simplified equation from the text, Qp/Qs can
be calculated based on the given information.
Qp/Qs ¼ ½SaO2  SvO2 =½SpvO2  SpaO2 
a Qp/Qs = [85%-65%]/[98%-65%] = 0.6
b Qp/Qs = [100%-75%]/[100%-75%] = 1.0
c Qp/Qs = [85%-65%]/[98%-75%] = 0.9
d Qp/Qs = [89%-65%]/[89%-65%] = 1.0
e Qp/Qs = [98%-65%]/[98%-80%] = 1.8
4. Which of the following is FALSE about a patient with a Glenn
anastomosis?
a. A low mixed venous saturation can be the result of hypoxia,
anemia, and low cardiac output
b. Systemic venous flow is divided between Glenn flow and
pulmonary venous flow
c. Hypoventilation is useful to improve oxygenation
d. The pressure in the SVC and PAs should be identical
e. Anything that decreases flow in the Glenn will cause
hypoxia
Answer: B
In patients with a Glenn anastomosis, Glenn flow and pul-
monary venous flow are equivalent, so answer B is incorrect. This
is because systemic venous flow from the SVC enters the PA via
the Glenn anastomosis, is oxygenated in the lungs and returns to
the common atrium via the pulmonary veins and therefore the
same flow goes through both. However, the IVC portion of sys-
temic venous flow enters directly into the common atrium, and
mixes with oxygenated pulmonary venous flow before entering
systemic circulation.
ET AL.
ACKNOWLEDGMENTS
Figures illustrated by Ryan Sun–Designer. Contact: hello@ryan-
sun.com
DISCLOSURES
The authors report no conflict of interest.
ORCID
Denise C. Joffe http://orcid.org/0000-0003-4729-0087
REFERENCES
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RECOMMENDED TEXTBOOK READING
5. Jonas R. Comprehensive Surgical Management of Congenital Heart Dis-
ease. London, UK: Arnold Publishers; 2004.
6. Rudolph A. Congenital Diseases of the Heart, 3rd edn. Oxford, UK:
John Wiley and Sons; 2009.
7. Cote CJ, Lerman J, Anderson BJ. A Practice of Anesthesia for Infants
and Children, 5th edn. Philadelphia, PA: Elsevier; 2013.
How to cite this article: Joffe DC, Shi MR, Welker CC.
Understanding cardiac shunts. Pediatr Anesth. 2018;00:1–10.
https://doi.org/10.1111/pan.13347