From the Biomedical Engineering Department, Tel Aviv University, Israel
(O.B.); the Department of Surgery, University of Louisville, Ky (W.P.S., E.S.,
S.C., E.H.A.); and the Division of Pediatric Cardiology, Mount Sinai Medical
Center, New York, NY.
Correspondence to Dr Ofer Barnea, Biomedical Engineering Department, Faculty of Engineering, Tel Aviv University, Ramat Aviv 69978, Israel.
Methods and Results—For the single-ventricle heart with both
circulations in parallel, we used a previously developed computer
simulation to obtain DO2 as a function of
systemic arterial (SaO2) and venous
(SvO2) oxygen saturation, arteriovenous oxygen
difference (Sa-vO2), or
pulmonary-to-systemic flow ratio (Qp/Qs). We also examined the
oxygen excess factor,
SaO2/Sa-vO2 (
Conclusions—Patients with low SvO2 values
require attention. Ideally, after reducing Qp/Qs to <1.5,
Management of neonates with hypoplastic left heart syndrome is complex
and controversial. Treatment generally commences with vigorous infusion
of prostaglandin to prevent the ductus arteriosus from
closing.3 This restores fetal parallel circulation, with
the right ventricle as the only active pump. However, reduction in
pulmonary resistance after birth may result in an unbalanced
circulation in which most blood flows into the pulmonary
circulation, thereby compromising systemic oxygen supply.
In a previous theoretical analysis,4 we examined
the effects of the ratio of pulmonary to systemic blood flow
(Qp/Qs) on systemic oxygen delivery (DO2). We
found that a Qp/Qs of <1 was optimal. However, maximizing oxygen
delivery based on Qp/Qs was difficult. Further, when calculating Qp/Qs
from blood gases, pulmonary venous oxygen saturation
(SpvO2) is generally estimated. This can lead
to substantial errors. Thus, in the present study, we examined
whether DO2 can be maximized by the use of
indices derived from oxygen saturation measurements.
In a previous study,4 we derived an equation for
DO2 based on the simple flow of oxygen uptake
in the lungs and whole-body oxygen consumption
(C
Buheitel et al6 proposed that an index of oxygen
delivery/oxygen consumption is helpful in managing infants with
critical cardiovascular problems. We refer to this
index as the oxygen excess factor
(SaO2/Sa-vO2 [
In computer simulations, a wide range of values can be examined. For
the results section, we selected 2 very different levels of
DO2. Setting the CO to 300 mL ·
min-1 · kg-1 simulated the low level
of DO2, whereas setting the CO to 450 mL
· min-1 · kg-1 simulated the high
level of DO2. Assuming a body surface area of
0.25 m2 for a 3.0-kg newborn, this gave a range in cardiac
index from 3.6 to 5.4 L · min-1 ·
m-2.
Figure 2
Figure 3
Figure 4
Figure 5A
Compared with the other indices, Qp/Qs provides
physiological information regarding the relative
pulmonary (Qp) and systemic (Qs) flows. One disadvantage of
Qp/Qs is that the value for SpvO2 is generally
estimated, and this estimation can cause errors in calculating Qp/Qs.
Based on Equation 7
Figure 6
Clinical Implications
The one disadvantage of
Based on this analysis and discussion, one strategy for
perioperative management of patients with hypoplastic
left heart syndrome might be to measure SaO2
and SvO2. Patients with low
SvO2 values require immediate attention. An
elevated estimated Qp/Qs ratio would indicate excessive Qp. Ideally,
after reducing the estimated Qp/Qs<1.5,
Comparison to Literature
We used this model to examine the response to inotropic agents in the
univentricular circulation.10 The response to
inotropic agents depended upon the agent. Dobutamine (15
µg · kg-1 · min-1) increased
the Qp/Qs ratio (1.03 to 2.52), while epinephrine (0.1
µg · kg-1 · min-1) decreased
the Qp/Qs ratio (1.23 to 0.82). Associated with these changes,
dobutamine decreased DO2 from 50 to
36 mL O2 per minute, while epinephrine increased
DO2 from 40 to 56 mL O2 per minute.
If we apply the index
Buheitel et al6 examined the ability of
SvO2 and
Seear et al11 examined the oxygen consumption-delivery
relationship in children. In stable children with normal lactate
levels, they found no significant rise in oxygen consumption when
oxygen delivery was increased by erythrocyte transfusion. Conversely,
infusion of adrenaline increased both consumption and
DO2. Berman et al12 examined
oxygen transport in patients with congenital heart disease. They found
that DO2 varied in direct relation to CO, but
not with arterial oxygen content.
DO2 varied with
SvO2.
The oxygen extraction ratio is also predictive of outcome. Rossi et
al13 studied 49 infants after congenital heart surgery.
The infants were intubated, paralyzed, and sedated with a continuous
infusion of fentanyl. Arterial blood gas data and mixed
venous oxygen saturation were measured on admission to the intensive
care unit and at 6 hours and 24 hours. Severe derangements in the
oxygen extraction ratio were present in nonsurvivors at 6 hours
after admission to the intensive care unit.13 Infants with
an oxygen extraction ratio >0.5 at 6 hours were at a much greater risk
of dying.
Limitations of Study
Obviously, care should always be taken in extrapolating from a
theoretical analysis to a clinical situation. One concern is
the measurement of mixed venous oxygen saturation. To measure the
saturation of mixed venous blood, samples must be recovered from a
central site at which all systemic venous blood is fully
mixed.15 In a theoretical model, this is easy to achieve.
However, in a neonate with hypoplastic left heart syndrome, it is
impossible to achieve. The pulmonary artery (or, after the
Norwood procedure, the neoaorta) contains both oxygenated
and deoxygenated blood. The right atrium also contains both
oxygenated and deoxygenated blood. This
necessitates sampling in the superior or inferior vena
cava. The great veins generally are not used for central venous
sampling, because the relative saturations of the superior and
inferior venae cavae differ greatly with
hemodynamic status.16 With no other choice
remaining, blood samples must be obtained from the vena cava, and
although this blood is not a truly mixed sample, it should
represent trends. By convention, the saturation in the superior
vena cava has been used by most pediatric cardiologists as a reflection
of the mixed venous oxygen saturation.
Summary
Received February 23, 1998;
revision received May 20, 1998;
accepted June 3, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Estimation of Oxygen Delivery in Newborns With a Univentricular Circulation
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—The management of neonates with complex congenital
anomalies depends on careful interpretation of arterial
blood gas values. Improved interpretation of these oxygen
parameters may allow clinicians to avoid unexpected
cardiovascular events. This study examined whether
systemic oxygen delivery (DO2) can be maximized
by the use of indices derived from oxygen saturation measurements in
neonates with hypoplastic left heart syndrome. 
). We
found that (1) slight increases in SaO2 may be
associated with large decreases in DO2. (2) Low
values for SvO2 indicate low values for
DO2. (3) Curves for
Sa-vO2 and Qp/Qs are redundant in the data
provided. (Qp/Qs, however, provides these data in more
physiologically relevant terms.) (4) High
values for Qp/Qs (>4) are associated with low
DO2. (5) Estimating Qp/Qs from oxygen
saturation measurements may result in errors when pulmonary
venous oxygen saturation is not available. (6) Maximizing
DO2 is extremely difficult using
SaO2, SvO2, and Qp/Qs.
(7) A linear relationship exists between and
DO2, and this linear relationship is not
altered by changes in cardiac output. might be
a better index to guide further therapy and maximize
DO2. Interventions that increased would be
considered beneficial, whereas interventions that decreased would
be considered detrimental.
Key Words: computers • hypoplastic left heart syndrome • hemodynamics • oxygen • pediatrics
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Hypoplastic left heart syndrome is presently the most
common cardiac malformation that results in death in
newborns.1 Without treatment, 95% of these infants die
during the first month of life, and none survive beyond 4
months.2
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
A model of flow in the univentricular circulation is
shown in Figure 1
. This diagram
represents the circulation of the newborn with hypoplastic left
heart syndrome that has been treated to maintain both atrial and
arterial shunts open. Pulmonary venous return is
forced into the right atrium, and right ventricular output
is distributed between pulmonary and systemic circulations.
This forms two parallel circulations.
View larger version (21K):
[in a new window]
Figure 1. A model of the circulation with hypoplastic left
heart syndrome. The darkened left ventricle (LV) indicates that the
ventricle is not functioning and that blood does not flow through it. P
indicates pulmonary circulation; S, systemic circulation; and
RV, right ventricle. 
O2). The analysis is based on
movement of oxygen into the pulmonary circulation (uptake) and
out of the systemic circulation (consumption). The basic equation is as
follows:
Equation 1
(1) 
states that the oxygen flow rate into the systemic
circulation (CaO2 · Qs) is reduced by
(CO2), leaving the reduced oxygen flow
rate returning to the right ventricle
(CvO2 · Qs).
Equation 2
(2) states that the oxygen flow rate into the
pulmonary circulation (CaO2 ·
Qp) plus oxygen uptake in the lungs
(SO2) gives the oxygen flow rate
returning to the right ventricle (CpvO2
· Qp). Equation 3 relates blood flow in the two circulations to total
cardiac output (CO):
The analysis assumes steady-state conditions, and thus
oxygen uptake and consumption must be equal:
(3)
By combining equations 1 to 4
(4) , DO2 (or
CaO2 · Qs) equals
Thus, DO2 is a complex function of CO,
pulmonary venous blood oxygen content
CpvO2 rate of
C
(5) O2 and Qp/Qs. Qp/Qs, based on the Fick
principle, can be expressed in a single-ventricle heart with parallel
circulation as
where SpvO2,
SvO2, and SaO2 are
pulmonary venous, systemic venous, and systemic
arterial oxygen saturation, respectively.
SaO2 and SvO2 levels
can be measured. However, SpvO2 is difficult to
measure and is generally estimated.5 To determine the
error involved in calculating Qp/Qs based on this estimation, the
derivative of equation 6
(6) with respect to SpvO2
is taken. Thus, the sensitivity (
) of Qp/Qs to
SpvO2 (or the relative change in Qp/Qs that is
generated by a small change in SpvO2) is
for example, when SpvO2 is 87.3% and
arterial oxygen saturation is 77%,
(7) =87.3/(87.3-77)=-8.5. This means that a 10% overestimation of
SpvO2 will result in a 85% underestimation of
Qp/Qs and vice versa. For example, with a SaO2
of 77% and a SvO2 of 45%, one may assume that
SpvO2 is 96% when it is actually 87.3%. The
calculated values of Qp/Qs would be 1.68, whereas the actual value for
Qp/Qs is 85% greater, or 3.11. This indicates that calculating Qp/Qs
by the use of equation 6 and assuming a value for
SpvO2 involves a risk of large errors. ]),
which can be calculated on the basis of 2 measurements of oxygen
saturation:
Using a computer (Compaq Computer Corp), we used the above
equations to determine the relationship of
SaO2, SvO2,
arterial-venous oxygen difference
Sa-vO2, Qp/Qs, and
(8) versus
DO2. The blood oxygen content was converted to
percent oxygen saturation by assuming a hemoglobin of 15 g/dL, giving
an O2 capacity of 22 mL O2 per dL blood
(1.38x15 per hemoglobin). CO2 was set
at 9 mL oxygen per minute per kilogram, which represents an
average value for neonates after cardiac surgery.7 8
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Figure 2 plots
SaO2 against DO2. Two
curves are presented: 1 with a lower level of
DO2 and the other with a higher
DO2. Both curves demonstrate a nonlinear
relationship between delivery and saturation. As
SaO2 increases, oxygen delivery increases,
reaches a peak, and then decreases rapidly. Peak oxygen delivery occurs
at Qp/Qs<1. For Qp/Qs>1, slight increases in
SaO2 can be associated with large decreases in
oxygen delivery. For example, for the higher oxygen delivery curve,
increasing SaO2 from 80% to 85% decreases
oxygen delivery from 34.1 to 14.6 mL O2 per minute per
kilogram. However, this doesn't mean that increasing
SaO2 is always associated with a decrease in
oxygen delivery. For example, going from the lower oxygen delivery
curve at an arterial oxygen saturation of 65% to the upper
oxygen delivery curve at an arterial oxygen saturation of
70% increases oxygen delivery from 24.0 to 45.0 mL O2 per
minute per kilogram.
View larger version (14K):
[in a new window]
Figure 2. Systemic arterial oxygen saturation
versus systemic oxygen (O2) delivery. Two curves are
presented. The curves were generated by setting the CO at 300
or 450 mL · min-1 · kg-1 and
varying Qp/Qs from 0.2 to 10. Most patients will have Qp/Qs>1. The
short line on each curve represents the point at which Qp/Qs=1.
Note that similar low and high oxygen delivery curves can be generated
with many combinations of CO, SpvO2, and
C O2. also shows that for any given SaO2, a
range of values exists for oxygen delivery. For example, at an
SaO2 of 70%, oxygen delivery can range from
21.9 mL to as much as 45.0 mL O2 per minute per
kilogram, depending on the CO. Additionally, no 1 value of
SaO2 exists at which oxygen delivery peaks. For
the upper curve, oxygen delivery peaks at 45.4 mL O2 per
minute per kilogram at an arterial oxygen saturation of
64%, whereas for the lower curve, a peak oxygen delivery of 24.6 mL
O2 per minute per kilogram occurs at an
arterial oxygen saturation of 60%. plots
SvO2 against DO2. Both
curves show a nonlinear relationship between oxygen delivery and
SvO2. However, for Qp/Qs>1, increases in
SvO2 are associated with increases in oxygen
delivery. Values of SvO2<40% are indicative
of severe derangements in oxygen transport (that is, the relationship
between oxygen delivery versus demand). While potentially related to an
increase in oxygen demand in the face of normal oxygen delivery in the
immediate postoperative period, a SvO2<40%
usually reflects a critical decrease in DO2.
Higher SvO2 values are associated with higher
DO2 values. However, for each curve, peak
oxygen delivery does not occur at the peak
SvO2. Further, even without a change in CO, the
same SvO2 value can be associated with two
possible values for oxygen delivery, depending upon the Qp/Qs value.
For example, for the higher oxygen delivery curve, a
SvO2 of 50% can have a
DO2 of 44.9 mL O2 per minute per
kilogram when Qp/Qs=0.38 or 22.5 mL O2 per minute per
kilogram, when Qp/Qs=2.68.
View larger version (13K):
[in a new window]
Figure 3. Systemic oxygen (O2) delivery
against SvO2. plots
Sa-vO2 versus DO2. As
with the other plots, a nonlinear relationship exists between oxygen
delivery and Sa-vO2. An
Sa-vO2>40 (ie, occurs at Qp/Qs>3) implies
very low levels of oxygen delivery irrespective of the CO level. For
Qp/Qs>1, as Sa-vO2 decreases, oxygen delivery
increases. As Sa-vO2 continues to decrease,
oxygen delivery peaks. Beyond this peak, oxygen delivery decreases
rapidly even though the Sa-vO2 continues to
decrease. For any given value for Sa-vO2, a
range of values exist for oxygen delivery. For example, at an
Sa-vO2 of 20, oxygen delivery ranges from 23.8
to 35.7 mL O2 per minute per kilogram depending on the CO.
Also, no 1 Sa-vO2 value exists for peak
DO2. For the upper curve, oxygen delivery peaks
at an Sa-vO2 of 12.7 (45.4 mL ·
min-1 · kg-1), whereas peak oxygen
delivery for the lower curve lies at an Sa-vO2
of 21.8 (24.6 mL · min-1 ·
kg-1).
View larger version (15K):
[in a new window]
Figure 4. Systemic oxygen (O2) delivery against
Sa-vO2. plots
DO2 versus Qp/Qs. Once again, the relationship
between oxygen delivery and Qp/Qs is nonlinear. For Qp/Qs>4, oxygen
delivery levels are very low and can only be partially compensated by
higher levels of CO. As Qp/Qs decreases toward 1, oxygen delivery
increases and peaks at values of Qp/Qs<1. If Qp/Qs continues to fall,
oxygen delivery precipitously decreases. For any given value of Qp/Qs,
a range of oxygen delivery values exists, and no single value for Qp/Qs
can predict an absolute peak in oxygen delivery.
View larger version (15K):
[in a new window]
Figure 5. A, Systemic oxygen (O2) delivery versus
Qp/Qs, B, Qp/Qs and its sensitivity as a function of estimated
SpvO2. Two curves are shown, one for a 5%
overestimation of SpvO2, the other for a 10%
overestimation of SpvO2. The analysis
assumes a SaO2 of 77% and a
SvO2 of 45%. The error in calculating the
Qp/Qs ratio depends on both the error in estimating and the actual
value of SpvO2. , the errors in the calculated values of Qp/Qs as a
function of SpvO2 are plotted in Figure 5B. The
figure shows that for the same percentage error in
SpvO2, the calculation error of Qp/Qs is
significantly larger at low values of SpvO2.
For example, at the highest level of SpvO2 a
minimal error of 5% (estimating SpvO2 as 95%
instead of the actual value of 90%) will yield a 25% error in the
calculated Qp/Qs. Estimating SpvO2 as 88% when
the actual value is 84% will result in a 60% error in Qp/Qs. A more
specific example is when SaO2 is 77% and
SvO2 is 45%, with an assumed
SpvO2 of 96%; the calculated Qp/Qs would be
1.68. If, however, the actual value for SpvO2
was 91.4% (a 5% overestimation), the actual Qp/Qs would be 2.22. For
a 10% overestimation of SpvO2 (87.3% versus
96%), the actual Qp/Qs would be 3.11.
plots the DO2
versus . Compared with the other relationships, a linear
relationship exists between DO2 and . As
increases, DO2 increases in a linear fashion,
and the higher , the higher the DO2.
Further, despite the large differences in CO, all the points lie on the
same line. For the lower CO (300 mL · min-1
· kg-1), the points lie on the lower left side of the
line at the lower levels of DO2. For the higher
CO (450 mL · min-1 · kg-1), the
points lie on the upper right side of the line.
View larger version (11K):
[in a new window]
Figure 6. Systemic oxygen (O2) delivery versus
(SaO2/Sa-vO2).
Light dashed line with Xs represents values obtained with a CO
of 300 mL · min-1 · kg-1. Heavy
dashed line represents values obtained with a CO of 450 mL
· minK-1 · kg-1.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
The management of neonates with complex congenital anomalies such
as hypoplastic left heart syndrome depends on careful interpretation of
arterial blood gas values. Improved interpretation of these
oxygen parameters may allow clinicians to avoid unexpected
cardiovascular events. Thus, we used a previously
developed computer simulation to obtain DO2 as
a function of SaO2,
SvO2, SvO2, and
Qp/Qs.4 Additionally, based on work by Buheitel et
al,6 we examined . The primary findings are as
follows:
and
DO2, and this linear relationship is not
altered by changes in CO and SpvO2.
The is based only on systemic oxygen saturation measurements
and reflects relative excess oxygen delivery.6 The is
calculated as SaO2 divided by
Sa-vO2, and it is the ratio of oxygen delivery
to oxygen consumption (the reciprocal of the oxygen-extraction ratio).
Compared with the other relationships, a linear relationship exists
between DO2 and . As increases,
DO2 increases in a linear fashion, and the
higher the , the higher the DO2. Thus,
irrespective of CO and SpvO2, high values
are associated with high levels of DO2. This
suggests that may be a better index to use to maximize
DO2. is that the slope of versus
DO2 varies with oxygen consumption (see Figure 7). Situations that increase DO2 but have
greater percentage increases in oxygen consumption would reduce the
even though total DO2 increased. Again, is
the relative excess in DO2. The implications of
an increase in DO2 with a decrease in needs
further consideration.
View larger version (12K):
[in a new window]
Figure 7. Systemic oxygen delivery (O2) versus
(SaO2/Sa-vO2). Two
lines are presented. For both lines, the CO was 450 mL ·
min-1 · kg-1. For one line,
CO2 was set at 9 mL oxygen per minute
per kilogram, which might represent the situation shortly after
surgery with the neonate sedated and partially paralyzed.7
For the other line, CO2 was set at 18 mL
oxygen per minute per kilogram. As is apparent in this example,
changing CO2 effects the slope of the
relationship between DO2 and . would guide further
therapy to maximize DO2. Interventions that
increased would be considered beneficial, whereas interventions
that decreased would be considered detrimental.
We have recently developed a stable, closed heart model of a
univentricular heart. We used neonatal pigs (3.5 to 6.0 kg)
to anastomose a Gore-Tex graft from the innominate artery and to the
pulmonary artery. We created an atrial septostomy by using a
Rashkind septostomy catheter. Occluding the right
ventricular outflow tract completed a
univentricular circuit in which all CO exited from the left
ventricle and the pulmonary circulation was maintained via flow
through the innominate artery-to-pulmonary artery
shunt.9 to these data, we can derive the same
conclusions: dobutamine decreased from 1.96 to 1.86,
while epinephrine increased from 1.63 to 2.22. to estimate cardiac index. They
studied 25 infants and children with biventricular
pathophysiology in the postoperative period after complete repair of
congenital heart disease. Cardiac index was calculated using the Fick
principle. SvO2 provided a reasonable estimate
of cardiac index. However, provided the best estimate of cardiac
index.
This analysis is based on a few simple equations
describing the flow of oxygen in the univentricular
circulation. The analysis showed that
DO2 is a complex function of CO,
CpvO2, CO2, and
the Qp/Qs ratio. For given values of Qp/Qs, CO, and
SpvO2, the analysis can predict the
DO2. However, the analysis cannot
describe how these values for Qp/Qs, CO, and
SpvO2 are achieved; nor can it predict the
whole body response to a change in one variable. For example, a
decrease in SpvO2 may increase
pulmonary vascular resistance, improve the Qp/Qs ratio, and
lead to an increased DO2. A more complex model
of the circulation is needed to predict whole-body responses to changes
in the variables.14
This study examined whether DO2 can be
maximized by the use of indices derived from oxygen saturation
measurements in neonates with hypoplastic left heart syndrome. We used
a previously developed computer simulation to obtain
DO2 as a function of
SaO2, SvO2,
Sa-vO2, and Qp/Qs. We also examined the .
Because of nonlinear relationships, maximizing
DO2 is extremely difficult by
SaO2, SvO2, or Qp/Qs.
However, a linear relationship exists between and
DO2, and this linear relationship is not
altered by changes in CO and SpvO2. Ideally,
after reducing Qp/Qs<1.5, might be a better index to guide further
therapy and maximize DO2.
Acknowledgments
This study was supported in part by a grant from the Alliant
Community Trust Fund.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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J. M. Pearl Right ventricular-pulmonary artery connection in stage 1 palliation of hypoplastic left heart syndrome J. Thorac. Cardiovasc. Surg., November 1, 2003; 126(5): 1268 - 1270. [Full Text] [PDF]
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T. Kitaichi, F. Chikugo, T. Kawahito, T. Hori, Y. Masuda, and T. Kitagawa Suitable shunt size for regulation of pulmonary blood flow in a canine model of univentricular parallel circulations J. Thorac. Cardiovasc. Surg., January 1, 2003; 125(1): 71 - 78. [Abstract] [Full Text] [PDF]
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S. Tabbutt, C. Ramamoorthy, L. M. Montenegro, S. M. Durning, C. D. Kurth, J. M. Steven, R. I. Godinez, T. L. Spray, G. Wernovsky, and S. C. Nicolson Impact of Inspired Gas Mixtures on Preoperative Infants With Hypoplastic Left Heart Syndrome During Controlled Ventilation Circulation, September 18, 2001; 104(90001): I-159 - 164. [Abstract] [Full Text] [PDF]
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R. Taeed, S. M. Schwartz, J. M. Pearl, J. L. Raake, R. H. Beekman III, P. B. Manning, and D. P. Nelson Unrecognized Pulmonary Venous Desaturation Early After Norwood Palliation Confounds Gp:Gs Assessment and Compromises Oxygen Delivery Circulation, June 5, 2001; 103(22): 2699 - 2704. [Abstract] [Full Text] [PDF]
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D J PENNY and L S SHEKERDEMIAN Management of the neonate with symptomatic congenital heart disease Arch. Dis. Child. Fetal Neonatal Ed., May 1, 2001; 84(3): 141F - 145. [Full Text]
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G. M. Hoffman, N. S. Ghanayem, J. M. Kampine, S. Berger, K. A. Mussatto, S. B. Litwin, and J. S. Tweddell Venous saturation and the anaerobic threshold in neonates after the Norwood procedure for hypoplastic left heart syndrome Ann. Thorac. Surg., November 1, 2000; 70(5): 1515 - 1520. [Abstract] [Full Text] [PDF]
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J. Rychik, D. M. Bush, T. L. Spray, J. W. Gaynor, and G. Wernovsky Assessment of pulmonary/systemic blood flow ratio after first-stage palliation for hypoplastic left heart syndromeDevelopment of a new index with the use of doppler echocardiography J. Thorac. Cardiovasc. Surg., July 1, 2000; 120(1): 81 - 87. [Abstract] [Full Text] [PDF]
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D. P. Francis, K. Willson, S. A. Thorne, L. C. Davies, and A. J. S. Coats Oxygenation in Patients With a Functionally Univentricular Circulation and Complete Mixing of Blood : Are Saturation and Flow Interchangeable? Circulation, November 23, 1999; 100(21): 2198 - 2203. [Abstract] [Full Text] [PDF]
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M. Poullis, O. Barnea, W. P. Santamore, A. Rossi, E. Salloum, S. Chien, and E. H. Austin Estimation of Oxygen Delivery in Newborns With a Univentricular Circulation • Response Circulation, August 10, 1999; 100 (6): 685 - 688. [Full Text] [PDF]
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D. P. Francis, L. C. Davies, A. J. S. Coats, O. Barnea, W. P. Santamore, A. Rossi, E. Salloum, S. Chien, and E. H. Austin Handling Complexity in Oxygen Delivery in the Univentricular Circulation • Response Circulation, July 13, 1999; 100 (2): 211 - 214. [Full Text] [PDF]
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