SUBDIAPHRAGMATIC VENOUS HEMODYNAMICS IN THE FONTAN CIRCULATION
From the Great Ormond Street Hospital for Children,NHS Trust, London,United Kingdom.
Supported by the National Science Foundation,USA.
Read at the Eightieth Annual Meeting of The American Association for Thoracic Surgery,Toronto,Ontario,Canada,April 30–May 3, 2000.
Dr Hsia is the recipient of the 1999 National Science Foundation
International Post-doctoral Research Fellowship Award,grant No. INT-9802808.
J Thorac Cardiovasc Surg 2001;121:436-47
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upright position over that in the supine position. A ratio of less than 1 implies a reduced Qnet in the upright position. Pressures. Twenty-five patients who underwent cardiac catheterization for various indications were studied 1 to 19 years (mean 6 ±5 years) after the Fontan operation. Eight of these patients (32%) were in self-reported New York Heart Association functional class I or II and the rest in class III or IV. Also,12 (48%) had IVC pressures (IVCP) more than or equal to 15 mm Hg. In terms of type of Fontan connection, 15 (60%) had total cavopulmonary connections and the rest atriopulmonary connections. Three patients had PLE. None had hepatic cirrhosis.
Catheterization data of 21 patients with normal right-sided cardiopulmonary anatomy were used as controls:16 patients with a hemodynamically trivial patent ductus arteriosus underwent elective device closure; 2 underwent routine review after heart transplantation; 2 with mild aortic stenosis were assessed for balloon dilatation; and 1 had a coronary angiogram for Kawasaki disease. In all subjects,the IVC, HV,and wedged HV pressures were measured in the supine position and during respiratory apnea to minimize effects of positive-pressure ventilation.
Among the Fontan patients,22 underwent both cardiac catheterization and flow measurements during the same hos-pital admission with Doppler measurements performed ini-tially. Of these,10 (45%) had IVCP more than or equal to 15 mm Hg (IVCP≥15). Data from these patients were compared with those with IVCP less than 15 mm Hg (IVCP<15). Within the IVCP<15 group,4 patients (33%) were in func-tional class I or II,whereas there were 3 (30%) in the IVCP≥15 group.
During elective cardiac catheterization under general anes-thesia,pressures in the subdiaphragmatic veins were mea-sured. These were recorded through a saline filled,balloon-tipped catheter (Kimal,Uxbridge,England) connected to a pressure transducer that was zeroed against atmospheric pres-sure and level with the mid chest. Measurements were made in the IVC,in one of the HVs,and in the “wedged”position within the HV by inflating the balloon. The wedged HV pres-sure correlates closely with directly measured PV pressure.10 Mean pressure values were obtained during respiratory apnea. In patients with atriopulmonary connections,because pressure tracing in the IVC and HV mirrors that in the right atrium,mean pressures were calculated by averaging the “a”wave and “v”wave. Difference between the mean wedged HV and free HV pressures was the transhepatic venous pres-sure gradient (TVPG).
Room air oxygen saturation was obtained from all Fontan patients with a pulse oximeter (Datex-Ohmeda,Madison, Wis). The study protocols were approved by the hospital research ethics committee and informed consents were obtained for all subjects.
Sta tistica l a na lysis. All data were expressed as mean ±standard deviation. For both flow and pressure data,differ-ences among various groups were assessed by 1-way analy-sis of variance with Neuman-Keuls multiple comparison test to evaluate all intergroup significance.
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but there was no difference in this inspiratory augmen-tation among the 3 groups.
HV flow in the Fontan groups was,however,more dependent on inspiration than in the control group; nei-ther progression to class III/IV nor higher IVCP enhanced or reduced this effect.
Control PV flow was higher during expiration (Fig 2). This expiratory augmentation was absent in all Fontan patients. Whereas in Fontan patients in NYHA class I the inspiratory and expiratory flow rates were nearly the same (Qin/Qex = 1.0),PV flow was the reverse of normal with higher flow during inspiration in those in class III/IV (Qin/Qex = 1.3). Similarly, accentuation of portal flow during inspiration was sig-nificantly more pronounced in IVCP≥15 than IVCP<15 patients.
Gravity effect. Although gravity did not have a sig-nificant influence on control IVC flow,it resulted in a similar 30% reduction in Fontan patients in both NYHA class I and class III/IV. There was no difference between the 2 IVCP groups.
Gravity reduced net flow in the control HV by 20%, but this reduction was more severe in both functional class groups,who lost an equivalent 40% of flow in the upright position. Comparing the 2 IVCP groups,howev-er,whereas the lower-pressure group’s flow reduction was the same (20%) as control,the decrement was sig-nificantly amplified (50%) in the higher-pressure group. In the PV,gravity lowered flow equally between controls and Fontan patients in NYHA class I,but progression to class III/IV resulted in a significant further decline with an approximately 50% reduction
Fig 2. Pulsed Doppler ultrasound recording with simultaneous respiratory monitoring from the portal vein in a con-trol subject,a Fontan patient in functional class I,and a Fontan patient in functional class III. Owing to its tortu-osity and anatomic variation,portal vein forward flow is recorded as a positive signal. Note the reduced velocities in control subjects but increased velocities in Fontan patients during inspiration.
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effects of the Fontan circulatory physiology and its sub-sequent deterioration on the subdiaphragmatic venous territory. This region is composed of 2 dynamically dis-tinct circulations:the splanchnic,which drains the gas-trointestinal tract through added resistance of the liver, and the systemic,which channels blood from the lower extremities and kidneys. In our previous study,6we described a transformation of respiratory and hydro-static influences on IVC,HV,and PV flow in the Fontan patients. In this article,our investigation revealed fur-ther profound but variable differences in both the flow and pressure dynamics in these venous territories between patients in functionally good condition and those in functionally poor condition.
B ecause the perceived functionality in the Fontan population correlates poorly with objective measures of cardiovascular performance,13we also examined the flow and pressure differences between Fontan patients with low and high systemic venous pressures. Mean right atrial pressure below 15 mm Hg is thought to be a “good”value in the Fontan circulation.11Chronic sys-temic venous hypertension is speculated to contribute to Fontan attrition,and increased pressure levels are associated with decreased functional performance and survival,as well as other complications.2,14Of note,in our study population,there were patients with report-edly good functional status but high caval pressures and vice versa. In addition,the length of postoperative follow-up was not different between the 2 pressure groups; thus,chronicity in a Fontan state does not seem to predict higher systemic venous pressure.
Instead of using maximal velocities or pulsatility ratios as indicators for flow dynamics in the subdi-aphragmatic venous circulation,15,16we calculated vol-umetric flow rate from Doppler recordings as a mea-sure of flow. Because the flow profiles in these veins are not symmetrically parabolic,instantaneous maxi-mal velocities cannot account for the continuous changes of flow throughout a cardiac or respiratory cycle. Similarly,degree of pulsatility does not yield dynamics pressure and flow information. In this study, volumetric flow rate is obtained by evaluating veloci-ties continuously with respect to time and assuming a constant cross-sectional area in all 3 veins throughout a respiratory cycle. Both the main HV and the IVC just distal to it are transhepatic in location and have been shown to remain in rigid configuration during all phas-es of respiration.17Furthermore,M-mode images of the PV diameter averaged over several cardiac cycles have produced agreement of ±0.5 mm with the instanta-
Fig 4. Analog recordings of the wedged (WHV) and free hepatic venous (HV) pressures in a control subject and a Fontan patient in functional class III. Note the normal transhepatic venous pressure gradient is nearly abolished in the Fontan patient. Also,the HV pressures are less pulsatile than normal in this patient who had a total cavopul-monary connection.
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neous diameter measured from B-mode imaging.8 Separate vein dimension measurements were obtained in supine and upright positions because there is no evi-dence for invariability with orthostasis.
Flow dynamics
Respiration. Respiratory modulation of venous return,or so-called cardiopulmonary interaction,has been known to occur when inspiratory negative intrathoracic pressure provides additional energy for forward flow. Comparison of this inspiratory augmen-tation of total venous return between normal subjects and Fontan patients has not been performed.18,19We have previously demonstrated in functionally well Fontan patients that cardiopulmonary interaction is amplified in the splanchnic circulation with minimal caval contribution. Our data here confirm this,showing that HV flow is mostly driven during inspiration. Thus, Fontan patients are likely to be more susceptible to dis-turbances to the respiratory mechanics such as diaphragm paralysis or significant pleural effusion, which need to be dealt with early. Interestingly,poor functional state or higher pressures required neither higher nor diminished respiratory drive for forward flow in the IVC or HV.
B lood flow in the normal PV is almost continuous except for a decrease during inspiration when the descending diaphragm transiently compresses the com-pliant and easily collapsible portal venules and hepatic sinusoids.20This is the site of resistance in the PV-HV axis.21In addition to maintaining a TVPG,this compli-ant resistance provides a passive mechanism for portal pressure autoregulation and for control of splanchnic capacitance response to changes in either central venous pressures or blood volume shifts.22,23The absence of this inspiratory reduction in Fontan patients suggests a decreased hepatic compressibility and reserve,where congested sinusoids act as fluid-filled columns that are always patent,allowing forward por-tal flow to occur during the same phase of respiration as its outflow,the HV. Sinusoidal dilatation and disten-tion are widely known characteristics of hepatic con-gestion in patients with severe right-sided heart fail-ure.24When systemic venous hypertension becomes worse,as in the IVCP≥15 group,more sinusoids become dilated,resulting in even higher PV flow dur-ing inspiration. Similarly,compared with class I, enhanced PV flow during inspiration in class III/IV may reflect a higher degree of sinusoidal congestion in the patients in functionally poorer condition. Gravity. Hydrostatic forces are known to constantly affect the intravascular pressures within the abdominal venous system.22Despite this,hydraulic changes caused by gravity are minimized in the systemic venous
circulation in human beings because of ventricular compensation,22as is illustrated by our control IVC data. In the Fontan patients,however,presumably because of the absence of a ventricular input,gravity had a more significant influence on IVC flow. Unlike the systemic blood flow,splanchnic venous blood flow has been found to decrease significantly in human beings during orthostasis.22,25This is also con-firmed by our results,which showed that gravity signif-icantly reduced net HV and PV flow rates in normal sub-jects. Because the splanchnic circulation is intrinsically susceptible to the adverse effect of hydrostatic forces, one might suggest that this is a vulnerable venous terri-tory to hemodynamic stress. Indeed,the splanchnic/ hepatic circulation,with its low mean transmural pres-sure and high capacitance,is subject to greater modifi-cation by external physical forces than almost any other regional circulation in the mammalian body.26 Compared with the normal physiology,the effects of gravity on splanchnic circulation in Fontan patients are variable:(1) HV flow reduction is amplified in all Fontan groups except those with low caval pressures and (2) PV flow decrement is more severe in all Fontan patients except those in good functional condition. In other words,in the face of hydrostatic influences,high-er systemic venous pressures result in poorer splanch-nic outflow,whereas poorer functional status correlates with worse portal drainage. During orthostasis,normal splanchnic circulation autoregulates against increased outflow resistance by sustained vasoconstriction.22Our data suggest that this mechanism is likely maintained in the HV when systemic venous pressure is low,and it is preserved in the PV when patients are functionally Fig 5. Transhepatic venous pressure gradient (TVPG) and inferior vena cava (IVC)pressure in 25 Fontan patients. There was a significant inverse correlation between TVPG and IVC pressure.
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well. However,in a failing Fontan circulation or one with high caval pressure,autoregulatory compensation appears to be overwhelmed,resulting in further decreased splanchnic flow and increased venous pool-ing. This poorer splanchnic flow dynamic may explain why so many of the late attritional complications are gastrointestinal in origin,such as ascites and PLE,both of which have been linked with splanchnic venous con-gestion.27,28
Pressure dynamics. To date,no study has evaluated the occurrence or extent of portal hypertension in Fontan patients. Normally,portal pressure ranges from 7 to 12 mm Hg and the pressure gradient between the PVs and HVs (TVPG) ranges from 1 to 4 mm Hg.10 Our control data agree closely with these values. Pressures above these limits classically define the pres-ence of portal hypertension and severity of cirrhosis. Fontan patients evaluated in this study have central venous,hepatic venous,and portal hypertension. Elevation of the central venous pressures in the Fontan circulation is a recognized inevitable consequence,and transmission of the caval and hepatic venous pressure to the portal vein is also well described.26Surprisingly,the normal gradient between venous inflow and outflow through the liver is abolished in Fontan patients in whom portal pressure mirrors the hepatic and caval pressures. So far as we know,diminished transhepatic gradient has not previously been linked with portal hypertension in human beings. Normally,the intrahe-patic vascular resistance at the sinusoidal level initially buffers the portal pressures from small changes in caval pressures,allowing only partial transmission of the ele-vated pressure.23However,as caval pressures continue to increase above the hepatic transmural pressure,the sinusoids are dilated and recruited to become an open tube system to allow synchronization of PV with HV flow,as well as pressure equalization.26,29,30In dogs, serial elevations of the IVC pressure resulted in pro-gressive increases in portal pressure,decreases in hepat-ic blood flow,and elimination of TVPG.31Furthermore, in patients with congestive heart failure and high right atrial pressures,TVPG is also reduced.32Nearly equal venous inflow and outflow pressures increase portal blood transit time through the liver,which together with enlarged hepatic blood volume due to higher outflow resistance results in congestion of the entire splanchnic macrocirculation and microcirculation.32,33Because the PV and HV are in direct pressure and flow communica-tion,it can be further speculated that in an atriopul-monary Fontan circulation,the observed HV regurgita-tion produced by atrial systole will place further stresses on the liver and gastrointestinal organs.16,34
Although our data suggest that patients in functional-
ly poorer condition have higher venous pressures and an even lower TVPG,progressively higher caval pres-sures significantly correlated with serially lower pres-sure gradients (Fig 5). Therefore,elevations of the sys-temic venous pressure lead to more hepatic congestion and portal hypertension,but deterioration of the Fontan circulation may not always predict transhepatic pres-sure equilibration.
Hepa tic dysfunction a nd PLE. Hepatic sinusoidal congestion/dilatation and subsequent cellular damage resulting from pressure effects35,36have long been rec-ognized as consequences of HV outflow obstruction, such as Budd-Chiari syndrome or chronic elevation of systemic venous pressures in congestive heart failure. Although acute congestion of the liver may lead to enzymatic dysfunction,chronic unrelieved sinusoidal congestion can produce diffuse irreversible parenchy-mal necrosis and fibrosis,or the so-called “cardiac cir-rhosis.”22,27,37This may explain the reported high inci-dence of hepatic dysfunction during late follow-up,3,12 significant correlation between raised systemic venous pressure with high aspartate transaminase levels,38and observations,within our institution and others,39of liver cirrhosis in the Fontan patient whose condition is deteriorating.
In addition to hepatic congestion,elevation of HV outflow pressure disturbs the balance of Starling forces governing passage of fluid across capillary walls and increases the trans-sinusoidal filtration of protein-rich hepatic fluids into the interstitium.27,30B ecause the hepatic sinusoids are highly permeable to proteins,26,33 even slight elevation in hepatic vascular pressure will lead to excessively high lymphatic filtration through the thoracic duct.29,40When impedance to systemic lym-phatic outflow increases,as in the Fontan circulation or congestive heart failure,lymphatic flow can reverse, finding a least-resistance path into the peritoneal cavity forming ascites,26,30,41or spill protein-rich lymph into the gut lumen.27PLE has been associated with other conditions in which splanchnic blood flow is impeded, such as other congenital heart diseases with high venous pressures and B udd-Chiari syndrome.38,42-45This hypothesis of PLE pathogenesis is further supported by direct correlation between increasing systemic venous pressures and fecal α
1
-antitrypsin levels in late sur-vivors of the Fontan operation.38Normal plasma protein levels can initially be maintained by compensatory increase in hepatic protein synthesis and decrease in catabolism,27explaining why some Fontan patients with
elevated fecal α
1
-antitrypsin have no clinical signs of PLE.38With further hepatic dysfunction resulting from
fibrotic changes and failure of the compensatory mech-anisms to keep pace with the enteric protein loss,hypoproteinemia and its sequelae will result.27
Limitations
In our previous study,we have characterized the dif-ferential physiology in patients with different types of Fontan connections. B ecause our focus here is on changes in flow and pressure dynamics between oppos-ing functional status,variations between Fontan con-nections were not examined.
Although Doppler ultrasound allows measurements of hepatic and portal volume flows with satisfactory relia-bility and reproducibility,8,46this method is known to be prone to error whenever the angle of insonation between the ultrasound beam and blood flow axis is not zero.7In our subjects,despite efforts to align the beam with the vessels,all had non-zero angles of incidence and correc-tion protocols were used. Yet,instead of comparing absolute values of flow rates,we calculated ratios of flow rates to evaluate the various effects using each sub-ject as his or her own control. In this manner,the cosine terms cancel each other and the error is neutralized.Conclusions
Usually subtle respiratory and gravitational influ-ences on subdiaphragmatic venous flow dynamics are profound and varied in patients who have had the Fontan operation. Unlike the normal,PV flow is aug-mented during the same phase of respiration as HV flow. Although progression to a worse functional state or elevation of the systemic venous pressure did not result in higher dependence on inspiration or worse hydrostatic effects in the IVC,splanchnic flow per-forms more poorly in the face of gravity. As a result of elevated central venous pressure,Fontan patients have portal hypertension but a reduced transhepatic gradient.The elimination of the pressure gradient is progressive-ly worse with higher caval pressures. These peculiar flow and pressure arrangements result in congestion of the entire PV-HV axis,including the sinusoids of the liver,which may adversely affect the long-term func-tion of the liver and gastrointestinal tract. Pharmaco-logic,interventional,and surgical modalities that opti-mize systemic venous pressure to allow adequate pulmonary blood flow without compromising splanch-nic venous return may prevent or reverse some of the late Fontan attrition complications such as PLE.
We thank the consultants and staff of the Cardiothoracic Unit at Great Ormond Street Hospital for Children for their support and cooperation.
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Received for publication May 4,2000; revisions requested Aug 9,2000; revisions received Sept 20,2000; accepted for publication Oct 24,2000.
Address for reprints:Marc R. de Leval,MD,FRCS,Cardiothoracic Unit,Great Ormond Street Hospital for Children,NHS Trust,Great Ormond St,London WC1N 3JH,United Kingdom (E-mail:hsia@https://www.wendangku.net/doc/3a13916915.html,).R E F E R E N C E S
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Discussion
Dr Hikaru Matsuda (Osaka,Japan). We have been con-ducting a similar study for patients who have had the Fontan operation in terms of PV or HV Doppler flow characteristics. We have found that the patients with higher central venous pressure have less PV flow.
I have 2 questions. First,what is the difference between the failing Fontan and the nonfailing Fontan states in terms of hemodynamics? Probably the patients with a failing Fontan circulation have higher venous pressure,and these are very reasonable results. Second,have you looked at the differ-ences regarding the types of cavopulmonary connection—the patients with atriopulmonary connection and total cavopul-monary connection? Our results indicate that pulsatile flow may worsen this effect for the hepatic circulation.
Dr Hsia.We have defined good and failing Fontan states by New York Heart Association functional class. In addition, of the Fontan patients studied,22 underwent both cardiac catheterization and Doppler measurements. These patients’flow dynamics were further divided into 2 groups:those with IVCPs less than 15 mm Hg and those with IVCPs more than or equal to 15 mm Hg,because pressures below 15 mm Hg had been described to be “good”values in a Fontan circula-tion.1On the basis of this criterion,while good functional state did not always indicate “good”hemodynamics and vice
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