(Circulation. 2001;103:2699.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Unrecognized Pulmonary Venous Desaturation Early After Norwood Palliation Confounds 
p:s Assessment and Compromises Oxygen Delivery
From the Divisions of Cardiology and Cardiothoracic Surgery, The Heart Center, Children’s Hospital Medical Center, Cincinnati, Ohio.
Correspondence to David P. Nelson, MD, PhD, Division of Pediatric Cardiology, Children’s Hospital Medical Center, 3333 Burnet Ave, OSB-4, Cincinnati, OH 45229-3039. E-mail davenelson{at}chmcc.org
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background—Hemodynamic stability after Norwood palliation often requires manipulation of pulmonary vascular resistance to alter the pulmonary-to-systemic blood flow ratio (
p:s). p:s is often
estimated from arterial saturation
(SaO2),
a practice based on 2 untested assumptions: constant systemic
arteriovenous O2 difference and normal
pulmonary venous saturation.
Methods and Results—In
12 patients early (
3 days) after Norwood palliation,
simultaneous arterial, superior vena caval
(SsvcO2),
and pulmonary venous
(SpvO2)
oximetry was used to test whether
SaO2
accurately predicts p:s. Stepwise multiple
regression assessed the contributions of
SaO2,
SsvcO2,
and
SpvO2
to p:s determination.
SaO2
correlated weakly with p:s
(R2=0.08,
P<0.05). Inclusion of
SsvcO2
and
SpvO2
improved p:s prediction accuracy.
Pulmonary venous desaturation
(SpvO2
<95%) was observed frequently (30%), especially at
FiO2
0.21, but normalized with higher
FiO2
or PEEP in all patients. In 6 patients,
FiO2
was increased incrementally from 0.17 to 0.50 to determine whether this
was an effective means to manipulate p:s.
p:s failed to change predictably with increased
FiO2.
In 5 of 6 patients, however, higher
SpvO2
and
SaO2
enhanced systemic oxygen delivery, as demonstrated by improvement in
oxygen extraction.
Conclusions—SaO2
correlated poorly with p:s because of variability
in
SsvcO2
and
SpvO2.
A novel observation was that pulmonary venous desaturation
occurred frequently early after Norwood palliation but normalized with
higher
FiO2
or PEEP. Because unrecognized pulmonary venous desaturation
confounds p:s assessment and compromises
SaO2
and oxygen delivery, judicious use of inspired oxygen and PEEP may be
beneficial in selected patients early after Norwood
palliation.
Key Words: heart defects, congenital • lung • surgery • hypoplastic left heart syndrome • Norwood operation
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Hemodynamic stability in the early postoperative period after Norwood palliation for hypoplastic left heart syndrome is largely dependent on maintaining a balance between pulmonary blood flow (
p) and systemic blood
flow (s).1
Ventilation strategies that alter pulmonary vascular resistance
are routinely used to manipulate the ratio of p to
s
(p:s).1 2
Estimation of the p:s ratio is thus vitally
important for accurate assessment of an unstable
hemodynamic state and to determine the effects of
interventions designed to alter the p:s. It has
long been accepted that arterial oxygen saturation
(SaO2)
is reflective of p:s after the Norwood
operation.2
The assertion that p:s can be
estimated from
SaO2
alone in single-ventricle physiology is based on a simplification of
the Fick equation that is not well founded. Because p is
supplied by a systemic-to–pulmonary artery shunt,
pulmonary and systemic arterial oxygen saturations
are equivalent, so that p:s can be calculated as
p:s=(SaO2-SmvO2)/(SpvO2-SaO2),
where mv is mixed-venous and pv pulmonary venous. This equation
has been further simplified on the basis of 2 untested assumptions: (1)
that systemic arteriovenous oxygen saturation difference (
A-V
O2) is constant (commonly assumed to be 
25),
and (2) that the pulmonary venous (PV) blood is fully
oxygen saturated (ie,
SpvO2
95%).1
These assumptions yield the simplified equation:
p:s=25/(95-SaO2).
This equation has been used to estimate p:s from
SaO2
alone.
The ability to determine p:s from
SaO2
is highly desirable, given the ease with which
SaO2
can be obtained in clinical practice. The assumptions that underlie
this simplified Fick equation may be false, however, in the immediate
postoperative Norwood period. A-V O2 will be
significantly greater than 25 if systemic blood flow is low, a common
occurrence in the postoperative period. Rossi and
colleagues3 4
reported the importance of monitoring superior vena cava (SVC) oxygen
saturation
(SsvcO2)
after Norwood palliation as a means of assessing s. The
assumption that PV blood is fully saturated has never been tested in
the postoperative Norwood circulation; however, it is a potentially
dangerous assumption, given the routine use of minimal inspired oxygen
(even subambient oxygen) and controlled hypercarbia in postoperative
management of these infants. Failure to account for a decrease in
SpvO2
will result in an important underestimation of
p:s based on
SaO2
alone. If reduced levels of inspired oxygen result in PV desaturation
without a significant decrease in p:s, the
associated decrease in
SaO2
may be detrimental to overall systemic oxygen delivery.
The purpose of this study was to use
simultaneous oximetry of arterial, SVC, and PV
blood to test the hypothesis that
SaO2
alone is an accurate predictor of p:s in the
early postoperative Norwood circulation. We thus hoped to evaluate the
validity of common assumptions regarding A-V
O2 and
SpvO2
in postoperative Norwood patients. A second aim was to determine
whether changes in fraction inspired oxygen
(FiO2)
are an effective means to alter
p:s.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Enrollment
Infants with single-ventricle anatomy and aortic arch obstruction undergoing stage I Norwood palliation with functional SVC and PV catheters were eligible for inclusion. These catheters are routinely placed intraoperatively during the Norwood procedure at our institution. Exclusion criteria included weight <2 kg, clinical or radiographic evidence of pulmonary disease, or the inability to draw samples from SVC or PV catheters. The study was approved by the Institutional Review Board of Children’s Hospital Medical Center, and informed consent was obtained from a parent or legal guardian before the study.
Intraoperative Procedure
A narcotic anesthetic was used for optimal myocardial
function. After sternotomy and bypass initiation, dissection was
completed during cooling. An atrial septectomy was performed via
atriotomy, the aortic arch was reconstructed with a homograft
patch,2 5 and the
pulmonary artery bifurcation was closed primarily. Retrograde
cardioplegia was administered during circulatory arrest. A
Gore-tex shunt was placed during rewarming.
Intracardiac catheters were inserted by the transatrial approach and
the tips directed into the SVC and left lower pulmonary vein
under direct visualization.
Postoperative Management
Patients were returned to the Cardiac Intensive Care
Unit with open sternotomy on a fentanyl infusion
and neuromuscular blockade. Postoperative monitoring included atrial
and systemic arterial pressures, ECG, pulse oximetry, and
end-tidal CO2. Patients were ventilated with
volume control ventilation at a tidal volume of 20 mL/kg and positive
end-expiratory pressure (PEEP) of 4 cm H2O. The
ventilator rate was adjusted to control
PaCO2.
Inotropic support and volume were administered as needed.
Diuretic therapy was initiated routinely on the first morning
after surgery.
SaO2,
SpvO2,
SsvcO2,
and p:s
Simultaneous oximetry of
arterial, SVC, and PV blood was performed as clinically
indicated in all patients with functional SVC and PV catheters. Because
there is no site to sample true mixed-venous blood in patients with
single-ventricle physiology, blood sampled from the SVC line was
considered the mixed-venous sample. It was also assumed that samples
from the left lower pulmonary vein were
representative of overall PV blood. To reduce potential
erroneous sampling of atrial blood, the SVC and PV lines were cleared,
and samples were drawn slowly with 1-mL syringes (unit protocol). True
p:s was determined as
(CaO2-CsvcO2)/(CpvO2-CaO2),
where
CaO2
is arterial oxygen content
(1.36xHgbxSaO2),
CsvcO2
is mixed-venous oxygen content
(1.36xHgbxSsvcO2),
and
CpvO2
is PV oxygen content
(1.36xHgbxSpvO2+0.003xPpvO2).
Hemoglobin was determined oximetrically for each data set. Estimated
p:s was determined from
SaO2
alone by the formula
25/(95-SaO2).
A-V O2 was determined as
CaO2-CsvcO2,
and the oxygen extraction ratio was determined as
(CaO2-CsvcO2)/CaO2,
where
CaO2
and
CsvcO2
represent arterial and mixed-venous oxygen content,
respectively.
FiO2
Effects on p:s
To determine whether changes in
FiO2
are an effective means to alter true p:s, data
were collected in a subset of patients as
FiO2
was systematically manipulated. Patients were studied 48 to 72 hours
after surgery, when gas exchange and hemodynamics were
steady state, usually just before sternal closure. Chest radiograph
confirmed the correct position of intracardiac catheters and absence of
pulmonary parenchymal changes. No manipulations in inotropic
support or minute ventilation were made during the changes in
FiO2.
After administration of fentanyl (10 µg/kg) and
vecuronium (0.1 mg/kg) and endotracheal tube
suctioning, baseline oximetric data
(SaO2,
SsvcO2,
and
SpvO2)
were obtained at an
FiO2
of 0.21. Hemodynamic and oximetric data were
subsequently collected as
FiO2
was adjusted incrementally to 0.17, 0.21, 0.30, and 0.50. Hemoglobin
was measured for each oximetric data set. After each change in
FiO2,
patients were allowed 10 minutes for equilibration before oximetric
data were collected.
Oximetric data were analyzed to determine the
effects of changes in
FiO2
on p:s. As surrogates of systemic oxygen
delivery, alterations in A-V O2 and the
oxygen extraction ratio were examined.
Data Analysis and Statistical
Methods
Data were analyzed with Statview software
(Abacus Concepts). For the purpose of correlating
SaO2
with true p:s, all measurements were assumed to
be independent, and stepwise linear multiple regression was used to
determine the contributions of
SaO2,
SsvcO2,
and
SpvO2
to the determination of p:s. Data are
presented as mean±SD. Statistical significance was defined as
a value of
P<0.05.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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From April 1997 to December 1998, 20 patients underwent Norwood palliation at Children’s Hospital Medical Center. Twelve patients were included in this study. Of the remaining 8 patients, there was 1 intraoperative death, 1 patient weighed <2 kg, and another patient developed Gram-negative sepsis/pneumonia. In 5 patients, the PV or SVC catheter was not placed successfully or could not be used for sampling, including 1 patient who was excluded because of atrial contamination of PV blood, as evidenced by SpvO2 data that closely approximated the SaO2. Oximetric data from the 12 study patients were used to test the assumptions underlying the simplified Fick equation, and in 6 of these patients, FiO2 was systematically altered to determine the effect of FiO2 on
p:s. One patient was not studied at subambient
oxygen
(FiO2=0.17)
because of significant PV desaturation during baseline room air
ventilation.
Patient characteristics are summarized in the
Table
.
The median age at the time of surgery was 7 days (range 3 to 45 days).
The median weight was 3.23 kg (range 2.2 to 4.1 kg). During the study
period, 14 of 20 neonates (70%) were discharged home and subsequently
returned for successful bidirectional Glenn anastomosis. Of the 12
infants included in the study, 2 infants died in the early
postoperative period and 1 died 2 months after the Norwood procedure of
persistent hepatic failure. All nonsurviving infants demonstrated
marked pulmonary overcirculation, demonstrating the highest
maximum p:s measurements recorded. Excessive
pulmonary blood flow in these patients was associated with
clinically important PV desaturation. PV desaturation
(SpvO2<95%)
was observed in 11 of 12 patients but normalized with higher
FiO2
or PEEP in all patients.
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Prediction of p:s From
SaO2
A total of 115 complete, simultaneous sets
of oximetric data
(SaO2,
SsvcO2,
and
SpvO2)
were available for analysis. True p:s
calculated from simultaneous oximetry data ranged from 0.45
to 5.43 and correlated poorly with
SaO2
(R2=0.08,P<0.05). There is a particularly poor correlation between
true p:s and
SaO2
at arterial saturations of 65% to 85%, where one might
expect a "balanced" circulation on the basis of the usual clinical
assumptions
(Figure 1).
|
Stepwise linear regression using
SaO2,
SsvcO2,
and
SpvO2
to predict p:s showed significant improvement in
ability to estimate p:s with inclusion of each
additional variable.
SaO2
alone accounted for only 8% of the variation in
p:s
(R2=0.08),
a remarkably low finding. Addition of
SsvcO2
increased this to 56%, and the PV component accounted for the
remaining variability in
p:s.
Systemic A-V
O2
The mean A-V O2 in the 115
samples was 30±11% (95% CI 8% to 52%). There was wide intrapatient
and interpatient variability, with a range of 9% to 50%. Variation in
SsvcO2
contributed most significantly to alterations in systemic A-V
O2. Consistent with the observations of
previous investigators,3 our
data indicate that variability in the systemic A-V
O2 confounds bedside assessment of
p:s from
SaO2
alone.
PV Desaturation Is Common in the Early
Postoperative Period After Norwood Palliation
Measured
SpvO2
ranged from 76% to 100%, and PV desaturation (defined as
SpvO2
<95%) was observed in 35 of the samples (30%).
SpvO2
was <90% in 17 of the 115 samples (15%). All but 1 patient had 1
desaturated PV sample, and 8 of 9 samples taken during administration
of subambient oxygen were <95%. Although PV desaturation was observed
more frequently at lower
FiO2,
it was also observed in 5 samples at
FiO2
of 0.30
(Figure 2). Desaturation of PV blood occurred without
evidence of pulmonary edema, atelectasis, or infiltrates or
catheter migration on repeated chest radiographs.
|
To verify that these were true PV samples and not samples
contaminated with atrial blood, an effort was made to normalize
SpvO2
in all patients who exhibited PV desaturation. By use of a combination
of increased
FiO2
and PEEP,
SpvO2
was raised to 95% in all patients, and
PpvO2
was >200 mm Hg in all patients studied at an
FiO2
of 0.50. The minimum and maximum
SpvO2
values for each individual patient are displayed in the
Table
,
and the interventions used to normalize
SpvO2
are noted.
FiO2
and p:s
As
FiO2
was increased,
SaO2
increased in all patients
(Figure 3, top). The corresponding PV blood, which was
desaturated in 5 of 6 patients at 0.17
FiO2,
became fully saturated as
FiO2
was increased
(Figure 3, second panel). Somewhat surprisingly, no
significant relationship between
FiO2
and p:s was observed with systematic manipulation
of
FiO2
(Figure 3, middle panel). As
FiO2
was increased from 0.17 to 0.50, only 1 patient (
symbols)
demonstrated a clinically important increase in
p:s with apparent reduction in systemic
O2 delivery (increased A-V
O2, decreased O2
extraction ratio). Although the systemic-pulmonary shunt in
this patient (patient 1,
Table)
was not excessively large, it is relevant that this patient had the
highest p:s on subambient oxygen of all patients
studied, suggesting excessive baseline pulmonary blood flow. In
the remaining 5 patients, systematic increases in
FiO2
failed to cause a corresponding change in p:s. In
these patients, changes in p:s and A-V
O2 with
FiO2
were minimal, but a reduced O2 extraction ratio
in these patients suggested more luxuriant systemic
O2 delivery
(Figure 3, lower 3 panels). Improvement in
SpvO2
at higher
FiO2
helped to enhance oxygen delivery, demonstrating the importance of
fully saturated PV blood to help optimize
SaO2
and systemic oxygen delivery. These data support the supposition that
decreases in pulmonary vascular resistance may have minimal
effect on p:s in patients in whom the
aortopulmonary shunt limits pulmonary blood flow
mechanically.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The fragile early postoperative course after Norwood palliation is exquisitely sensitive to the balance of systemic and pulmonary blood flow.1 2 6 7 Bedside estimation of
p:s from
SaO2
alone has been advocated on the basis of 2 untested assumptions:
constant systemic A-V O2 and normal
SpvO2
(95%). This study demonstrates that
SaO2
is a poor predictor of p:s after Norwood
palliation;
SaO2
alone predicted only 8% of the variability in
p:s. Inaccuracy in p:s
estimation was caused by variability in both
SmvO2
and
SpvO2,
thus challenging the dual assumptions used by clinicians for rapid
bedside assessment of p:s. Although others have demonstrated variability in SmvO2 after Norwood palliation,3 8 this is the first study to demonstrate that PV desaturation is also common. PV desaturation was observed in 30% of PV samples even though there was no evidence of pulmonary edema, atelectasis, or infiltrates on chest radiograph. The data thus suggest that postoperative Norwood patients may have pulmonary gas exchange abnormalities resulting from cardiopulmonary bypass, circulatory arrest, and the extensive surgical procedure. Furthermore, ventilatory maneuvers used to manipulate pulmonary vascular resistance in these patients (ie, controlled hypoventilation, low FiO2) may predispose patients to microatelectasis and ventilation-perfusion mismatch.
The presence of unrecognized PV desaturation may contribute
to substantial errors in p:s estimated from
SaO2
alone. The data indicate that p:s is
underestimated at higher levels of true p:s, when
it is most clinically relevant
(Figure 4A). Our observations
(Figure 4B) provide clinical evidence to substantiate the
computer modeling predictions of Barnea and
colleagues.6 7 If
PV blood is assumed to be fully saturated (95%), the error in
p:s estimation can be substantial if true
SpvO2
falls below 95%. p:s is underestimated by 20%
to 25% when
SpvO2
is 90%, and the underestimation error is as large as 30% to 70% if
SpvO2
falls below 90%. The data also suggest that the frequency and degree
of PV desaturation may be intensified by use of reduced levels of
FiO2
(Figures 2 and 3), as commonly used in the
perioperative management of single-ventricle patients.
Reduced or subambient
FiO2
can lower
SaO2
by decreasing
SpvO2
without a concomitant decrease in p:s. The
resultant decrease in systemic oxygen delivery may not be recognized,
because the patient is assumed to be "better" on the basis of the
decrease in
SaO2.
|
The observation that high
FiO2
and/or a mild respiratory alkalosis after Norwood palliation may not
result in significant hemodynamic instability is
supported by the work of Mosca and
colleagues.9 Our data support
the conjecture that p:s may be insensitive to
manipulations in pulmonary vascular resistance when the
systemic-to-pulmonary shunt limits pulmonary blood flow
mechanically. As
FiO2
was systematically increased, we did not observe consistent
changes in p:s, and the oxygen extraction ratio
improved in 5 of 6 patients
(Figure 3). These findings support the judicious use of
higher PEEP and/or
FiO2
in select patients after Norwood palliation. In a similar manner, it
may not be beneficial to aggressively induce respiratory acidosis in
all postoperative Norwood patients, because controlled hypoventilation
may predispose patients to microatelectasis and ventilation-perfusion
mismatch. Because clinical recognition of PV desaturation is difficult
in the absence of a pulmonary vein catheter, the consequences
of any ventilatory maneuvers must be assessed cautiously by determining
their effect on
SaO2
and
SmvO2
and global end-organ perfusion.
The conclusions of this study are contingent on accurate
sampling of PV blood. To verify that atrial contamination of PV samples
was minimal, an effort was made to normalize
SpvO2
in all patients exhibiting PV desaturation. With a combination of
increased
FiO2
and PEEP,
SpvO2
was raised to 96% in all patients, and the PV
PO2
was >200 mm Hg in all patients studied at an
FiO2
of 0.50
(Table).
The substantial improvements in PV
PO2
with increases in
FiO2
and/or PEEP indicate minimal atrial contamination of PV samples.
Another limitation of the study is the assumption that SVC and PV
samples reflect
SmvO2
and mixed
SpvO2,
respectively. Although these assumptions are commonly used during
catheterization of single-ventricle patients, they may
be inaccurate. Finally, we would caution that the findings should not
be generalized too broadly. These data represent only a small
sample of postoperative Norwood patients, and the observations reported
are specifically relevant to the early postoperative period. The data
should be interpreted carefully and should not be applied broadly to
all single-ventricle patients. Low-level or subambient inspired oxygen
is presumably not detrimental for patients with preoperative
single-ventricle physiology and healthy lungs in whom pulmonary
blood flow is limited by pulmonary vascular resistance alone. We do not
advocate use of high
FiO2
in single-ventricle patients with obvious pulmonary
overcirculation, especially those with preoperative single-ventricle
physiology. Similarly, unnecessarily high PEEP in single-ventricle
patients may reduce venous return and thus be detrimental to overall
cardiac output.
In summary, this study demonstrates that systemic
SaO2
alone is a poor predictor of p:s in the early
postoperative period after Norwood palliation. Because inaccuracy in
p:s estimation resulted from variability in both
SsvcO2
and
SpvO2,
the data challenge the dual assumptions used by clinicians for rapid
bedside assessment of p:s. The novel observation
that PV desaturation is common in the early postoperative period after
Norwood palliation raises the possibility that undetected
pulmonary gas exchange defects may adversely affect systemic
oxygen delivery in some patients after Norwood palliation. Because
unrecognized PV desaturation confounds p:s
assessment and compromises
SaO2
and oxygen delivery, judicious use of inspired oxygen and PEEP in the
early postoperative period after Norwood palliation may be beneficial
in selected
patients.
|
Acknowledgments |
|---|
This study was supported by The Children’s Heart Association of Cincinnati.
Received February 15, 2001; revision received March 21, 2001; accepted March 26, 2001.
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T. Nakano, H. Kado, Y. Shiokawa, K. Fukae, Y. Nishimura, K. Miyamoto, Y. Tanoue, H. Tatewaki, and N. Fusazaki The low resistance strategy for the perioperative management of the Norwood procedure Ann. Thorac. Surg., March 1, 2004; 77(3): 908 - 912. [Abstract] [Full Text] [PDF]
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G. M. Hoffman, J. S. Tweddell, N. S. Ghanayem, K. A. Mussatto, E. A. Stuth, R. D. B. Jaquis, and S. Berger Alteration of the critical arteriovenous oxygen saturation relationship by sustained afterload reduction after the norwood procedure J. Thorac. Cardiovasc. Surg., March 1, 2004; 127(3): 738 - 745. [Abstract] [Full Text] [PDF]
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S. M. Bradley, A. M. Atz, and J. M. Simsic Redefining the impact of oxygen and hyperventilation after the Norwood procedure J. Thorac. Cardiovasc. Surg., February 1, 2004; 127(2): 473 - 480. [Abstract] [Full Text] [PDF]
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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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K. O. Maher, C. Pizarro, S. S. Gidding, K. Januszewska, E. Malec, W. I. Norwood Jr, and J. D. Murphy Hemodynamic Profile After the Norwood Procedure With Right Ventricle to Pulmonary Artery Conduit Circulation, August 19, 2003; 108(7): 782 - 784. [Abstract] [Full Text] [PDF]
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J. S. Tweddell, G. M. Hoffman, K. A. Mussatto, R. T. Fedderly, S. Berger, R. D. B. Jaquiss, N. S. Ghanayem, S. J. Frisbee, and S. B. Litwin Improved Survival of Patients Undergoing Palliation of Hypoplastic Left Heart Syndrome: Lessons Learned From 115 Consecutive Patients Circulation, September 24, 2002; 106(12_suppl_1): I-82 - I-89. [Abstract] [Full Text] [PDF]
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