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(Circulation. 1997;96:3934-3942.)
© 1997 American Heart Association, Inc.
Articles |
Cardiopulmonary Interactions After Fontan Operations
Augmentation of Cardiac Output Using Negative Pressure Ventilation
From the Departments of Paediatrics (L.S.S., A.B., A.N.R.) and Surgery (D.F.S., C.L.), Royal Brompton Hospital, London SW3 6NP, UK.
Correspondence to Prof A. Redington, Professor of Congenital Heart Disease, Royal Brompton Hospital, Sydney St, London SW3 6NP, UK. E-mail reding{at}ibm.net
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Abstract |
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Background The low-output state is the chief cause of morbidity and mortality after Fontan operations. An alternative hemodynamic tool would be a welcome addition for these patients, who are typically resistant to conventional therapeutic measures.
Methods and Results The hemodynamic effects of conversion from conventional intermittent positive pressure ventilation (IPPV) to cuirass negative pressure ventilation (NPV) was investigated in nine acute postoperative Fontan patients on the pediatric intensive care unit and nine anesthetized patients undergoing cardiac catheterization in the convalescent phase after Fontan operations. Pulmonary blood flow was measured using the direct Fick method during IPPV and after a brief period of NPV. In one subgroup of patients, pulmonary blood flow was measured again after reinstitution of IPPV, and in a second subgroup, pulmonary blood flow was measured after an extended period of NPV. A brief period of NPV increased pulmonary blood flow from 2.4 to 3.5 L · min-1 · /m-2, with a mean increase of 42%. Pulmonary blood flow continued to improve, with a total increase of 54% after an extended period of NPV. Values fell toward baseline after reinstitution of IPPV. Heart rate was unchanged during NPV, and the improvement in pulmonary blood flow was achieved by an increase in stroke volume from 25 mL/m2 to 37 mL/m.2
Conclusions Through improvement of the stroke volume alone, NPV brought about a marked increase in the pulmonary blood flow and, hence, cardiac output of Fontan patients. An improvement in cardiac output of this order, and by this mechanism, is currently unmatched by any therapeutic alternatives.
Key Words: Fontan procedure • cardiac output • ventilation
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Introduction |
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The Fontan operation and its modifications have remained an important milestone in the surgical management of selected patients with complex cyanotic congenital heart disease. In the original description of his operation in patients with tricuspid atresia, Fontan observed that the reduction in right atrial pressure that followed extubation was accompanied by a clinical improvement in all cases and concluded that spontaneous respiration should be established as early as possible in these patients.1 We now know that in the majority of Fontan patients, pulmonary blood flow, the main determinant of cardiac output, is a largely passive diastolic phenomenon that is strongly influenced by changes in intrathoracic pressure that are present during spontaneous and mechanical ventilation.2,3 Antegrade diastolic pulmonary arterial flow, and hence cardiac output, increases during spontaneous inspiration but is significantly lowered during positive pressure inspiration.4
Despite a number of modifications in surgical technique that have favorably influenced the early postoperative course of patients undergoing Fontan-like operations,5,6 the chief cause of morbidity and mortality in this group remains a low cardiac output state. A low cardiac output is not in itself a surprising feature in the immediate postoperative period, when the important influences of mechanical ventilation are superimposed on the inevitable global effects of cardiopulmonary bypass on the heart and lungs. However, reduced cardiorespiratory function has been demonstrated both at rest and during exercise in a number of late postoperative studies of Fontan patients,7–9 and it would appear that the pulmonary blood flow of patients in the late postoperative phase may be as sensitive to changes in the mean airway pressure as that of their acute counterparts.2,3 NPV has previously been shown significantly to increase Doppler-derived antegrade pulmonary arterial flow in a small number of anesthetized patients with an atriopulmonary connection10 and qualitatively in spontaneously breathing individuals after a total cavopulmonary connection.11
Furthermore, we previously reported a significant improvement in pulmonary blood flow during a brief period of NPV in a small number of children who were ventilated in the early postoperative period after right heart surgery.12
In this study, we compare the effects of IPPV and negative pressure ventilation in nine early postoperative Fontan patients and nine anesthetized patients undergoing cardiac catheterization in the late convalescent phase after Fontan-like operations so we can quantify the effects of these differing ventilatory strategies on the "Fontan" circulation.
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Methods |
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Patients
The hemodynamic effects of cuirass NPV were prospectively studied on 18 separate occasions in 14 paralyzed and fully sedated patients (8 males; median age, 6.3 years) who were initially receiving IPPV after Fontan-like operations. Nine studies were carried out in the immediate postoperative period and nine were carried out in the late postoperative (convalescent) phase after elective cardiac catheterization with the patients under general anesthesia. Four patients were studied in both the acute and convalescent phases. Pulmonary blood flow was measured using the direct Fick method in all cases.
Acute Patients
Nine children (4 boys; median age, 5.8 years) were studied on
the pediatric intensive care unit at the Royal Brompton Hospital
between 4 and 14 hours after a fenestrated total cavopulmonary
connection. This is our procedure of choice, with the inclusion of a
fenestration in the lateral tunnel being independent of preoperative
hemodynamics. All patients had indwelling
peripheral arterial catheters and
pulmonary arterial and pulmonary venous
catheters that were inserted intraoperatively.
Anthropometric data, diagnoses, details of previous palliative
procedures, and inotropic support at the time of study are given in
Table 1
.
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Convalescent Patients
Nine paralyzed and fully sedated patients (4 males; median age,
6.7 years) were studied under while general anesthesia
after elective cardiac catheterization between 5 months
and 15 years after an atriopulmonary connection (3 patients) or
total cavopulmonary connection (6 patients). Details of
surgery, interval since surgery, and indications for cardiac
catheterization are given in Table 2.
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Patients 1* through 4* and 14 were studied after successful transcatheter closure of a surgical fenestration using a 17-mm umbrella device (Bard). Complete occlusion was confirmed with angiography at the end of the procedure in all cases. Patient 10 did not have evidence of baffle obstruction either angiographically or in terms of directly measured pressure gradients under anesthesia and so fulfilled the criteria for inclusion in the study. Patient 13 had a right-to-left shunt through a inferior baffle leak, and it was not possible to occlude this with a transcatheter technique.
Criteria for Inclusion
All patients were in sinus rhythm at the time of study, and no
patient had evidence of anatomic obstruction to the "Fontan
pathway" or overt systemic ventricular dysfunction. All
convalescent patients were in New York Heart Association functional
class I or II.
Ventilation
All patients were intubated with a cuffed endotracheal tube
(Mallinckrodt Medical). IPPV was delivered using a Servo ventilator
900C (Siemens), and NPV was delivered using the Hayek external
high-frequency oscillator. This consists of an appropriately sized
flexible Perspex cuirass that fits over the patient's chest and upper
abdomen from the level of the clavicles to the level of the umbilicus.
Ventilatory adjustments are made from a bedside power unit, to which
the cuirass is attached. In this study, the Servo ventilator was used
to deliver oxygen and a small amount of additional pressure support (3
to 5 cm H2O) during NPV to overcome the
inevitable resistance to gas flow presented by the endotracheal
tube. Ventilatory parameters during IPPV and NPV are
summarized in Table 3.
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Hemodynamic Monitoring
All patients had continuous surface ECG monitoring and
noninvasive monitoring of peripheral oxygen saturation,
oxygen consumption, and end-tidal carbon dioxide. Systemic blood
pressure, pulmonary arterial pressure, and (in
patients with a right-to-left shunt) pulmonary venous pressure
were monitored invasively.
Hemodynamic Measurements
Pulmonary blood flow was measured using the direct Fick
method. Oxygen consumption was directly measured using respiratory mass
spectrometry as previously described.12,13 The
mass spectrometer inlets and argon (indicator gas) flow were calibrated
before each period of patient monitoring. Before commencement of steady
state monitoring, the cuff of the endotracheal tube was inflated to
eliminate any leak of respired gases; the oropharynx was then checked
for leaks by sampling for carbon dioxide with one of the mass
spectrometer sampling probes.
A prerequisite for the accurate and meaningful measurement of pulmonary blood flow using the direct Fick method is a cardiorespiratory steady state. Acute postoperative studies were not carried out within 4 hours of a patient's return from the operating theater. This delay ensured central rewarming in all cases and allowed sufficient time for adequate sedation, analgesia, and paralysis to be induced through continuous intravenous infusions. In addition, patients were not suctioned or moved during the entire study period, and doses of intravenous inotropes in the early postoperative patients were not altered. A cardiorespiratory steady state was defined as a 15-minute period during IPPV and before measurement of pulmonary blood flow during which patients were not spontaneously breathing or moving and did not display any changes in heart rate or blood pressure that might suggest insufficient sedation or analgesia. During this period, blood pressure, heart rate, oxygen consumption, and end-tidal carbon dioxide were required to not fluctuate by >5%.
In all cases, the mixed venous oxygen content was calculated from pulmonary arterial blood samples. All of the acute patients and patient 13 had a right-to-left shunt through a surgically created fenestration (patients 1 through 9) or an angiographically evident baffle leak (patient 13). In these patients, for the calculation of pulmonary blood flow, "arterial" oxygen content was calculated from pulmonary venous samples. Systemic arterial oxygen content was also measured to calculate the systemic blood flow and assess the right-to-left shunt fraction. In patients without a shunt (patients 10, 11, 12, and 14), arterial oxygen content was calculated from aortic samples. The pulmonary-to-systemic flow ratio was assumed to equal 1.0 in these patients.
Study Protocol
Standard Studies
The term "standard study" was used to define the
comparative, brief study protocol designed to assess the
hemodynamic effects of conversion from IPPV to NPV; the
outline for a standard study is shown in Fig 1A. In brief, at the end of a 15-minute
steady state period during IPPV (IPPV1),
pulmonary blood flow, and (in patients with a right-to-left
shunt) systemic blood flow were measured. NPV was then commenced using
an appropriate sized cuirass, and a second pulmonary blood flow
measurement was made after 15 minutes of NPV
(NPV1). Seventeen standard studies were
completed.
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Extended Studies
Patients in whom the study period was extended beyond the above
standard protocol outlined above constituted two subgroups:
Subgroup 1 (7 Patients, 3 Acute Patients). In
patients in subgroup 1, a third measurement of pulmonary blood
flow was made after IPPV was reinstituted at the end of a standard
study (IPPV2) to ensure that no bias was
introduced by the standard protocol that involved conversion from IPPV
to NPV, in that order. The outline for subgroup 1 patients is given in
Fig 1B
.
Subgroup 2 (6 Patients, 3 Acute Patients). In
patients in subgroup 2, the period of NPV was extended after the
completion of a standard study, and a third measurement of
pulmonary blood flow was made after a total of 30 to 45 minutes
of NPV (NPV2). This modification was chosen to
investigate the hemodynamic effects of a prolonged
conversion to NPV. The study outline is given in Fig 1C.
Statistical Analysis
Group data are expressed as mean±SD. Within-group data for all
patients during IPPV and NPV were compared using an ANOVA with
Bonferroni's correction for multiple comparisons. Statistical
comparisons between acute and convalescent patients were made using the
Mann-Whitney U test. In all cases, the null hypothesis was
rejected for values of P>.05.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In patient 9, the hemodynamic study could not be completed. The cuirass was easily fitted with an adequate seal, but the patient desaturated on the start of NPV. The possible reasons for this are discussed later.
Baseline Hemodynamic Data During
IPPV1
Baseline data for the two groups of patients during
IPPV1 are given in Table 4. There was no difference in the mean
oxygen consumption between acute and convalescent patients. In the
presence of a patent baffle fenestration in all acute patients, the
systemic arterial oxygen saturation was 
3% lower than
that in the convalescent group. The mixed venous saturation was much
lower in the acute patients (56.5±16.8%) than in the convalescent
group (70.2±5.8%; P=.03). The arteriovenous oxygen
difference for pulmonary blood flow (using pulmonary
venous samples for arterial oxygen content in patients with
a right-to-left shunt) was 7.4±2.7 mL/dL in acute patients and
5.3±1.3 mL/dL in convalescent patients (P=.03). The
arteriovenous oxygen difference for systemic blood flow (using systemic
arterial samples for arterial content in all
patients) was 6.5±3.0 mL/dL in acute patients and 5.5±1.4 mL/dL in
convalescent patients; this did not quite reach a level of statistical
significance (P=.07). Despite having a similar
arterial carbon dioxide tension, the acute patients had a
significantly greater metabolic acidosis than the
convalescent group.
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The mean Qp ranged from 0.56 to 4.6 L ·
min-1 · m-2 in the
acute patients, with a mean of 2.3 L ·
min-1 · m-2, and
from 1.5 to 4.8 L · min-1 ·
m-2 in the convalescent group, with a mean of
L · min-1 ·
m-2. There was no difference in baseline
Qp between the two groups (P=.4).
However, the acute patients were significantly more tachycardic than
the convalescents, and thus their baseline "systemic" stroke volume
index was much lower: 21.4 versus31.7 mL/m2
(P=.01; Fig 2).
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Standard Studies
With the exception of patient 9, all patients were ventilated
easily during NPV, maintaining stable systemic arterial
oxygen and carbon dioxide tensions. Results of standard studies are
given in Table 5. Mean oxygen consumption
for acute patients increased from 146±52 to 176±55 mL ·
min-1 · m-2 during
NPV1 (P=.01), and in convalescent
patients, it increased less markedly: from 125±35 to 136±30 mL
· min-1 · m-2
(P=.07). Oxygen consumption for the group as a whole
increased from 136±44 to 156±47 mL ·
min-1 · m-2 during
NPV1 (P=.01).
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The mixed venous oxygen saturations during both IPPV1 and NPV1 were significantly lower in acute than in convalescent patients (P=.03), but values increased significantly during NPV1 in both groups: from 56.6±16% to 60.2±19% in acute patients and from 70.2±5.8% to 77.4±5.4% in convalescents (P=.02 for both groups). The mean mixed venous saturation for all patients increased from 63.4±14% to 70.1±5.3% during NPV1 (P=.0009).
The arteriovenous difference in oxygen content decreased significantly in acute (P=.01) and convalescent (P=.03) patients during NPV1, and combined values for all patients decreased from 6.3±2.3 to 5.2±2.4 mL/dL (P=.0007).
Pulmonary blood flow increased during
NPV1 from 2.3±1.2 to 3.3±1.9 L ·
min-1 · m-2 in
acute patients and from 2.6±1 to 3.7±1.1 L ·
min-1 · m-2 in
convalescent patients (P=.01 for both groups).
Pulmonary blood flow during all standard studies (acute plus
convalescent) increased from 2.4±1.1 to 3.5±1.5 L ·
min-1 · m-2
(P=.0003, Fig 3), with a mean
increase of 42±24%. There was no significant difference in the
increase in pulmonary blood flow between acute and convalescent
patients.
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There was a slight decrease in pulmonary arterial pressure during NPV1 and this was statistically significant (P=0.003). Left atrial (or pulmonary venous) pressure was unchanged, and the pulmonary vascular resistance index decreased from 2.0±1.3 to 1.3±1.2 Wood units/m2 (P=.01).
Heart rate was unchanged during NPV, and stroke volume for the group as
a whole increased during NPV from 24.9±13 to 36.5±22
mL/m,2 with a mean increase of 44%
(P<.0001). The systemic stroke volume of the acute patients
increased from 21±8.8 to 27.2±13 mL/m2 during
NPV (P=.01), and increased from 31.7±13 to 48.4±21
mL/m2 in convalescent patients
(P<.01). The stroke volume was significantly lower for
acute patients during both IPPV1 and
NPV1 (P=.01; see Fig 2). The
right-to-left shunt fraction was unchanged during
NPV1.
Extended Studies
Subgroup 1:
IPPV1
NPV1IPPV2
The hemodynamic data for this subgroup are given
in Table 6. The mixed venous oxygen
saturation increased significantly during NPV1,
the increase in oxygen consumption was not significant, and
pulmonary blood flow increased by 43% (Fig 4). After IPPV was reinstituted
(IPPV2), all parameters tended to
return to baseline, with a significant reduction in mixed venous oxygen
saturation (P=.02) and a fall in oxygen consumption that did
not quite reach a level of statistical significance
(P=.08).
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Subgroup 2:
IPPV1NPV1NPV2
The data for this subgroup are given in Table 7. Mixed venous oxygen saturation and
oxygen consumption both increased significantly during
NPV1. Pulmonary blood flow in this
subgroup increased by 36.2% during NPV1, and
continued to do so during NPV2, with an ultimate
total increase of >53% during a 30- to 45-minute period of negative
pressure ventilation (Fig 5).
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Predictors of Hemodynamic Improvement During
NPV
The data from standard studies were examined to investigate any
possible predictors of the ultimate hemodynamic
improvement that could be achieved during NPV (Table 8). In the convalescent patients, there
was no correlation between the increase in Qp
during a standard study and pulmonary arterial
pressure, left ventricular end-diastolic
pressure, transpulmonary gradient, pulmonary vascular
resistance, or baseline Qp during
IPPV1. In the acute patients, patients with a
higher preoperative left ventricular
end-diastolic pressure (R=.83, P=.02)
and a higher postoperative pulmonary arterial
pressure (R=.87, P<.01) tended to derive a
greater improvement during NPV. Fig 6
shows the correlation between increase in pulmonary blood flow
and postoperative pulmonary arterial pressures in
the acute patients.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study showed that a brief period of cuirass NPV increased the pulmonary blood flow of patients with the Fontan circulation by 42% and that the improvement was not only sustained but further continued if the period of NPV was extended. The mixed venous saturation increased significantly, and improvement in cardiac output was achieved by an augmentation in stroke volume with the heart rate remaining constant.
Although pulmonary blood flow is a marker of total cardiac output, many of the patients in this study group had a significant right-to-left shunt, so pulmonary and systemic flow were not always equal. For this reason, before a discussion of clinical implications of the study, it is necessary to reemphasize that NPV did not alter the shunt fraction. In other words, the pulmonary blood flow did not increase at the "expense" of the systemic blood flow during NPV, so one can reasonably surmise that changes in pulmonary blood flow accurately represented changes in the systemic cardiac output.
Patient 9 could not effectively be ventilated using NPV. This child was receiving cyclical peritoneal dialysis and was one of the first patients on the intensive care unit to be included in this study. In retrospect, a likely explanation for poor gas exchange was that the increase in intraperitoneal fluid must have significantly compromised the potential for diaphragmatic movement—an important component of effective NPV. The use of continuous "cross-flow" peritoneal dialysis in subsequent cases in which children were receiving therapeutic NPV (not reported here) has reassuringly avoided the large shifts in intraperitoneal volume, allowing NPV to be effectively combined with supplementary renal support.
Baseline Hemodynamics
The baseline cardiac output of the acute and convalescent patients
during IPPV were very similar. Implicit in this comment lies the
inference that the convalescent patients had a low cardiac output. Why
should this be so? Was their cardiac output significantly reduced by
the very conservative levels of IPPV used in this study? This would
seem unlikely, and there was no reason why the cardiac output of
convalescent patients should have been any more affected by IPPV than
that of the acute patients. Furthermore, it is widely accepted that
Fontan patients have a lower resting cardiac output than healthy
individuals,14 and indeed the baseline cardiac
index and stroke volume of the ventilated convalescent patients in this
study are comparable to measurements made in other studies of
spontaneously breathing Fontan patients.14–16
The baseline values in this study were an expression of the
cardiovascular responses under very specific (and quite
different) conditions in the two subgroups. In the acute patients,
there was a higher resting metabolic demand with a
consequent need for an appropriate augmentation of cardiac output. This
response may, however, have been inadequate because this group had a
greater metabolic acidosis and higher arteriovenous oxygen
difference. The metabolic demands of the
anesthetized convalescent patients, who, in contrast, were not
acidotic and had a lower arteriovenous oxygen difference (and therefore
oxygen extraction), were presumably much less at the time of study, and
in the simplest terms, these patients may not "have needed" a
higher cardiac output. All of the acute patients were receiving
vasoactive drugs, and although these agents generally offer little
beneficial clinical effect on the systolic
ventricular function or the peripheral vascular
tone of Fontan patients, their presence would almost certainly have
contributed to the marked tachycardia. From this point
follows the observation that although the total pulmonary blood
flow was similar in both patient groups, the stroke volume of
convalescent patients was significantly higher than that of the
tachycardic acute patients, suggesting that there were important
differences both in the mechanisms for the maintenance of a
given cardiac output and for the degree of hemodynamic
reserve that was present in the two subgroups.
Mechanisms for Increases in Pulmonary Blood Flow During NPV
in Fontan Patients
The cardiac output of all individuals theoretically can be
improved by increasing the heart rate, stroke volume, or, indeed, both.
The cardiac output of children in general is more heart rate than
stroke volume dependent, but an exaggeration of this "normal"
phenomenon is seen in Fontan patients who even at rest tend to have a
faster heart rate than healthy control
subjects.17 Similarly, the chronotropic
augmentation of cardiac output in response to an increase in
metabolic demand—for example, during exercise or after
cardiopulmonary bypass—predominates. In contrast, an increase
in stroke volume in either response to endogenous demand or
by exogenous manipulation is much more difficult to achieve in Fontan
patients and is often unchanged or can even be reduced during
exercise.16–18 There are a number of potential
reasons for this. First, the systemic ventricle has been chronically
volume loaded preoperatively, and changes in ventricular
geometry19 and regional abnormalities of wall
motion20 after surgery affect systolic
and diastolic functions. Second, the combination of a
relatively high systemic venous pressure—a necessary driving force in
the Fontan circulation—and a generally low cardiac output results in
an elevated systemic vascular resistance, which by increasing the total
afterload limits the potential for an increase in stroke volume. In
addition, individual patients will be further limited if there is more
overt systemic ventricular dysfunction or their
pulmonary blood flow is restricted by conduit
obstruction,14 an abnormal pulmonary
vascular response, or an elevated left ventricular
end-diastolic pressure.
Clearly, however, this study tests the therapeutic benefits of manipulation of the interplay between pulmonary blood flow and spontaneous and mechanical ventilation in Fontan patients. It is now well known that spontaneous inspiration enhances pulmonary blood flow and stroke volume in both atriopulmonary and total cavopulmonary circulations.2,3 We previously speculated that the work of breathing may be one of the more significant sources of energy in the latter circulation, both at rest and during exercise.8 Given that these patients are normally so dependent on physiological respiration to maintain pulmonary blood flow, one might have expected to see an even greater enhancement of cardiac output than that seen during negative pressure ventilation. The first important observation was that in subgroup 2, the pulmonary blood flow continued to increase if the period of NPV was extended. Presumably, there must lie a plateau (which has not been demonstrated here) beyond which cardiac output can no longer continue to improve, and this maximal improvement may exceed that which we have shown. It would have been interesting to have further lengthened the period of NPV to explore this hypothesis. However, in the catheter laboratory, the constraints of time with patients under general anesthesia would not allow a longer study period. In the intensive care unit, the assumption of a steady state for a longer period so soon after cardiopulmonary bypass, aside from the fact that blood transfusion, colloid administration, or chest physiotherapy is often required, would have rightly exposed the protocol to criticism.
Nevertheless, in patients whose total cardiac output is normally so dependent on heart rate, an improvement of >50% in pulmonary blood flow and stroke volume alone coupled with a marked rise in mixed venous saturation is probably unmatched by any other current therapeutic alternative that is available and applicable to this complex group. In this study, the improvement in cardiac output during NPV was comparable to the maximal response demonstrated in exercising Fontan patients,15,18 further emphasizing the potential for exploitation of cardiac output during NPV.
Although the average rise in cardiac output was >50% in extended studies, the range of increase in cardiac output during NPV was between 10% and 100%. The individual response to NPV was difficult to predict. There was no relationship between the improvement in cardiac output during NPV and any hemodynamic parameters that we though may have influenced this in the convalescent patients. In the acute patients, however, possibly a very encouraging finding was that the improvement in pulmonary blood flow was completely independent of baseline pulmonary blood flow at the onset of the study. In addition, patients with a higher postoperative pulmonary arterial pressure seemed to benefit more from NPV. A similar relationship was seen in those patients who had a higher preoperative left ventricular end-diastolic pressure, underscoring the desirability of an improvement in diastolic filling of the ventricle by directly increasing pulmonary blood flow. One might speculate, therefore, that NPV may be of most benefit to patients who had higher risk factors for postoperative morbidity. It is important to mention, however, that all of the acute patients had relatively favorable postoperative hemodynamics, with no child having a pulmonary arterial pressure of >16 mm Hg.
Conclusions
Patients who have undergone Fontan-like operations often have
signs of a low cardiac output state in the early postoperative period.
Obviously in the presence of systemic ventricular
dysfunction, a degree of pharmacological myocardial and renal support
may be desirable, but often the unwanted side effects of inotropes,
such as an increase in pulmonary and systemic vascular
resistance or inappropriate tachycardia, are superimposed
on their positive hemodynamic influences. These effects
can be particularly detrimental to the sensitive Fontan circulation,
and a nonpharmacological approach may be very desirable under these
circumstances.
NPV improved the cardiac output of Fontan patients by manipulating the important cardiopulmonary interactions that exist in this patient group to produce a highly significant increase in stroke volume, the degree of which may be unrivaled.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This research was supported by the British Heart Foundation. I would like to thank Dr Michael Rigby and Dr Elliott Shinebourne for allowing us to study their patients. I would also like to thank Ray Matcham of Balzers UK for his technical support in using the mass spectrometer.
Received June 12, 1997; revision received August 6, 1997; accepted August 22, 1997.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-
Fontan F, Baudet E. Surgical repair of tricuspid
atresia. Thorax. 1971;26:240–248.[Medline]
[Order article via Infotrieve]
-
Penny DJ, Redington AN. Doppler
echocardiographic evaluation of pulmonary blood
flow after the Fontan operation: the role of the lungs. Br
Heart J. 1991;66:372–374.
[Abstract/Free Full Text]
-
Redington AN, Penny D, Shinebourne EA.
Pulmonary blood flow after total cavopulmonary shunt.
Br Heart J. 1991;65:213–217.
[Abstract/Free Full Text]
-
Williams DB, Kiernan PD, Metke MP, Marsh HM, Danielson
GK. Hemodynamic response to positive end-expiratory
pressure following right atrium-pulmonary artery bypass (Fontan
procedure). J Thorac Cardiovasc Surg. 1984;87:856–861.[Abstract]
-
de Leval MR, Kilner P, Gewillig M, Bull C. Total
cavopulmonary connection: a logical alternative to
atriopulmonary connection for complex Fontan operations.
J Thorac Cardiovasc Surg. 1988;96:682–695.[Abstract]
-
Bridges ND, Lock JE, Castaneda AR. Baffle fenestration
with subsequent transcatheter closure: modification of the
Fontan operation for patients at increased risk.
Circulation. 1990;82:1681–1689.
[Abstract/Free Full Text]
-
Harrison Dam Liu P, Walters JE, Goodman JM, Siu SC,
Webb GD, Williams WG, McLaughlin PR. Cardiopulmonary function
in adult patients late after Fontan repair. J Am Coll
Cardiol. 1995;26:1016–1021.[Abstract]
-
Rosenthal M, Bush A, Deanfield J, Redington A.
Comparison of cardiopulmonary adaptation during exercise in
children after the atriopulmonary and total
cavopulmonary connection Fontan procedures.
Circulation. 1995;91:372–378..
[Abstract/Free Full Text]
-
Driscoll DJ, Feldt RH, Mottam CD, Pura FJ, Scharr HV,
Danielson GK. Cardiorespiratory response to exercise after definitive
repair of univentricular atrioventricular
connection. Int J Cardiol. 1987;17:73–81.[Medline]
[Order article via Infotrieve]
-
Penny DJ, Hayek Z, Rawle P, Rigby ML, Redington AN.
Ventilation with external high frequency oscillation around
a negative baseline increases pulmonary blood flow after the
Fontan operation. Cardiol Young. 1992;2:277–280.
-
Penny DJ, Hayek Z, Redington AN. The effects of
positive and negative extrathoracic pressure ventilation after the
total cavopulmonary shunt procedure. Int J
Cardiol. 1991;30:128–130.[Medline]
[Order article via Infotrieve]
-
Shekerdemian LS, Shore DF, Lincoln C, Bush A, Redington
AN. Negative pressure ventilation improves cardiac output after right
heart surgery. Circulation. 1996;94(suppl II):II-49–II-55.
-
Davies NJH, Denison DM. The measurement of
metabolic gas exchange and minute volume by mass
spectrometry alone. Respir Physiol. 1979;36:261–267.[Medline]
[Order article via Infotrieve]
-
Ben Shachar G, Fuhrman BP, Wang Y, Lucas RV, Lock JE.
Rest and exercise hemodynamics after the Fontan
procedure. Circulation. 1982;65:1043–1048.
[Abstract/Free Full Text]
-
Driscoll DJ, Danielson GK, Puga FJ, Schaff HV, Heise
CT, Staats BA. Exercise tolerance and cardiorespiratory response to
exercise after the Fontan operation for tricuspid atresia or functional
single ventricle. J Am Coll Cardiol. 1986;7:1087–1094.[Abstract]
-
Zellers TM, Driscoll DJ, Mottam CD, Puga FJ, Schaff HV,
Danielson GK. Exercise tolerance and cardiorespiratory response to
exercise before and after the Fontan operation. Mayo Clin
Proc. 1989;64:1489–1497.[Medline]
[Order article via Infotrieve]
-
Gewillig MH, Lundstrom UR, Bull C, Wyse RKH, Deanfield
JE. Exercise responses in patients with congenital heart disease after
Fontan repair: patterns and determinants of performance.
J Am Coll Cardiol. 1990;15:1424–1432.[Abstract]
-
Driscoll DJ, Feldt RH, Mottam CD, Pura FJ, Scharr HV,
Danielson GK. Cardiorespiratory response to exercise after definitive
repair of univentricular atrioventricular
connection. Int J Cardiol. 1987;17:73–81.
-
Rychik J, Jacobs ML, Norwood WI. Acute changes in left
ventricular geometry after volume reduction operation.
Ann Thorac Surg. 1995;60:1267–1274.
[Abstract/Free Full Text]
-
Penny DJ, Rigby ML, Redington AN. Abnormal patterns of
intraventricular flow and diastolic
filling after the Fontan operation: evidence for incoordinate
ventricular wall motion. Br Heart J. 1991;66:375–378.
[Abstract/Free Full Text]
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