Cava Pressure Research Articles

Venovenous extracorporeal membrane oxygenation drainage cannula performance: From generalized to patient-averaged vessel model

Venovenous extracorporeal membrane oxygenation is used for respiratory support in the most severe cases of acute respiratory distress syndrome. Blood is drained from the large veins, oxygenated in an artificial lung, and returned to the right atrium (RA). In this study, we have used large eddy simulations to simulate a single-stage “lighthouse” drainage cannula in a patient-averaged model of the large veins and RA, including the return cannula. We compared the results with previous experimental and numerical studies of these cannulas in idealized tube geometries. According to the simulations, wall proximity at the drainage holes and the presence of the return cannula greatly increased drainage through the tip (33% at 5 L/min). We then simulated a multi-stage device in the same patient-averaged model, showing similar recirculation performance across the range of extracorporeal membrane oxygenation (ECMO) flow rates compared to the lighthouse cannula. Mean and maximum time-averaged wall shear stress were slightly higher for the lighthouse design. At high ECMO flow rates, the multi-stage device developed a negative caval pressure, which may be a cause of drainage obstruction in a clinical environment. Finally, through calculation of the energy spectra and vorticity field, we observed ring-like vortices inside the cannula originating from the side holes, most prominent in the proximal position. Our work highlights the important differences between a patient-derived and simplified venous model, with the latter tending to underestimate tip drainage. We also draw attention to the different dynamics of single-stage and multistage drainage cannulas, which may guide clinical use.

The clinical and hemodynamic characteristics of pulmonary hypertension in patients with OSA-COPD overlap syndrome

BackgroundOur study aimed to assess the clinical and hemodynamic characteristics of pulmonary hypertension (PH) in patients with overlapping obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD), referred to OSA-COPD overlap syndrome (OS). MethodsWe enrolled a total of 116 patients with OS, COPD, or OSA who underwent right heart catheterization (RHC) due to suspected PH. We conducted a retrospective analysis of the clinical and hemodynamic characteristics of these patients. ResultsAmong the three groups (OS group, n = 26; COPD group, n = 36; OSA group, n = 54), the prevalence of PH was higher in the OS group (n = 17, 65.4%)compared to OSA group (n = 26,48.1%) and COPD group (n = 20,55.6 %). Among three groups with PH, the superior vena cava pressure (CVP) and right ventricular pressure (RAP) were higher in the OS group than in the OSA group (P < 0.05). Patients in the OS and COPD groups had higher pulmonary artery wedge pressure (PAWP) than in the OSA group (14.88 ± 4.79 mmHg, 13.45 ± 3.68 mmHg vs. 11.00 ± 3.51 mmHg, respectively, P < 0.05). OS patients with PH exhibited higher respiratory event index (REI), time spent with SpO2 <90%, oxygen desaturation index (ODI), minimal SpO2 (MinSpO2) and mean SpO2 (MSpO2) compared to OS patients without PH. After adjusting for potential covariates, we found that MinSpO2 (OR 0.937, 95 % CI 0.882–0.994, P = 0.032), MSpO2 (OR 0.805, 95% CI 0.682–0.949, P = 0.010), time spent with SpO2 <90% (OR 1.422, 95% CI 1.137–1.780, P = 0.002), and FEV1 % pred (OR 0.977, 95 % CI 0.962–0.993, P = 0.005) were related to the development of PH. ConclusionsPatients with OS showed higher prevalence of PH, along with higher PAWP, CVP and RAP. Worse nocturnal hypoxemia was found in OS patients with PH.

Intraoperative transit-time flow measurement of caval veins before and after bidirectional cavopulmonary anastomosis.

Haemodynamic changes in caval venous flow distribution occurring during bidirectional cavopulmonary anastomosis operation are still largely unknown. Transit time flow measurements were performed in 15 cavopulmonary anastomosis operations. Superior and inferior caval vein flows were measured before and after the cavopulmonary anastomosis. Ratio of superior caval vein to overall caval veins flow was calculated. Mean superior caval vein flow ratio before cavopulmonary anastomosis was higher than previously reported for healthy children. Superior caval vein flow ratio decreased in 14/15 patients after cavopulmonary anastomosis: mean 0.63 ± 0.12 before versus 0.43 ± 0.14 after. No linear correlation between intraoperative superior caval vein pressure and superior caval vein flow after cavopulmonary anastomosis was found. Neither Nakata index nor pulmonary vascular resistance measured at preoperative cardiac catheterisation correlated with intraoperative flows. None of patients died or required a take down. The higher mean superior caval vein flow ratio before cavopulmonary anastomosis compared to healthy children suggests flow redistribution in univentricular physiology to protect brain and neurodevelopment. The decrease of superior caval vein flow ratio after cavopulmonary anastomosis may reflect the flow redistribution related to trans-pulmonary gradient. The lack of correlation between superior caval vein pressure and superior caval vein flow could be explained by limited sample size and multifactorial determinants of caval veins flow, although pressure remain essential. Larger sample of measurements are needed to find flow range potentially predictive for clinical failure. To authors' knowledge, this is the first intraoperative flow measurement of both caval veins during cavopulmonary operations.

Hemodynamic and recirculation performance of dual lumen cannulas for venovenous extracorporeal membrane oxygenation

Venovenous extracorporeal membrane oxygenation (ECMO) can be performed with two single lumen cannulas (SLCs) or one dual-lumen cannula (DLC) where low recirculation fraction ({R}_{f}) is a key performance criterion. DLCs are widely believed to have lower {R}_{f}, though these have not been directly compared. Similarly, correct positioning is considered critical although its impact is unclear. We aimed to compare two common bi-caval DLC designs and quantify {mathrm{R}}_{mathrm{f}} in several positions. Two different commercially available DLCs were sectioned, measured, reconstructed, scaled to 27Fr and simulated in our previously published patient-averaged computational model of the right atrium (RA) and venae cavae at 2–6 L/min. One DLC was then used to simulate ± 30° and ± 60° rotation and ± 4 cm insertion depth. Both designs had low {R}_{f} (< 7%) and similar SVC/IVC drainage fractions and pressure drops. Both cannula reinfusion ports created a high-velocity jet and high shear stresses in the cannula (> 413 Pa) and RA (> 52 Pa) even at low flow rates. Caval pressures were abnormally high (16.2–23.9 mmHg) at low flow rates. Rotation did not significantly impact {R}_{f}. Short insertion depth increased {R}_{f} (> 31%) for all flow rates whilst long insertion only increased {R}_{f} at 6 L/min (24%). Our results show that DLCs have lower {R}_{f} compared to SLCs at moderate-high flow rates (> 4 L/min), but high shear stresses. Obstruction from DLCs increases caval pressures at low flow rates, a potential reason for increased intracranial hemorrhages. Cannula rotation does not impact {R}_{f} though correct insertion depth is critical.

In Silico Evaluation of a Self-powered Venous Ejector Pump for Fontan Patients.

The Fontan circulation carries a dismal prognosis in the long term due to its peculiar physiology and lack of a subpulmonic ventricle. Although it is multifactorial, elevated IVC pressure is accepted to be the primary cause of Fontan's high mortality and morbidity. This study presents a self-powered venous ejector pump (VEP) that can be used to lower the high IVC venous pressure in single-ventricle patients. A self-powered venous assist device that exploits the high-energy aortic flow to lower IVC pressure is designed. The proposed design is clinically feasible, simple in structure, and is powered intracorporeally. The device's performance in reducing IVC pressure is assessed by conducting comprehensive computational fluid dynamics simulations in idealized total cavopulmonary connections with different offsets. The device was finally applied to complex 3D reconstructed patient-specific TCPC models to validate its performance. The assist device provided a significant IVC pressure drop of more than 3.2mm Hg in both idealized and patient-specific geometries, while maintaining a high systemic oxygen saturation of more than 90%. The simulations revealed no significant caval pressure rise (< 0.1mm Hg) and sufficient systemic oxygen saturation (> 84%) in the event of device failure, demonstrating its fail-safe feature. A self-powered venous assist with promising in silico performance in improving Fontan hemodynamics is proposed. Due to its passive nature, the device has the potential to provide palliation for the growing population of patients with failing Fontan.

Pentadecapeptide BPC 157 Counteracts Hemodynamic and ECG Disturbances Induced by Sotalol in Rats

Cytoprotective and organoprotective pentadecapeptide BPC 157 demonstrated particular beneficial cardiovascular effects (Curr Pharm Des. 2014;20(7):1121‐1125). Antiarrhythmic effects counteracted digoxin toxicity (Regul Pept. 2009;156(1‐3):83‐89), major blood vessel occlusions (Biomedicines 2021, 9,1029; 2021, 9,609; 2021, 9, 792) and lidocaine toxicity (Emerg Med Int. 2020;2020:6805354). Now, we reveal, by BPC 157, mitigation of hemodynamic and ECG disturbances of sotalol, a class III antiarrhythmic with non‐selective beta‐blocking activity.Albino Wistar rats received sotalol (80mg/kg, intragastrically), and at 5 min thereafter were treated with saline or BPC 157 (10ng/kg, intragastrically. Seven standard and one precordial ECG leads were recorded (baseline; after application of sotalol; and 10, 30, 90, 120 and 150 minutes after application of sotalol). Heart rate, QRS complex, PR and QT intervals were analyzed. Corrected QT intervals (QTc) were calculated according to Fridericia formula.Baseline ECG readings included average heart rate of 275.5 ± 25 bpm, average PR 54.8 ± 3.4 ms, average QRS complex 25.0 ± 4.23 ms and average QTc 166 ± 9.7 ms. Sotalol caused bradycardia (245 ± 23.5 bpm), PR prolongation (57.3 ± 2.7 ms), QRS widening (26.3 ± 3.2 ms), and QTc prolongation (173 ± 9.1 ms), measured 10 minutes after application. In BPC 157 treated animals (5 minutes after BPC‐157 application, 10 minutes after sotalol application), these effects were attenuated (heart rate 306 ± 31.7 bpm, average PR 52.3 ± 1.6 ms, average QRS 23.7 ± 5.4 ms and average QTc 159 ± 21.2 ms). This attenuation was lost in later measurements, for QRS ‐ 25 minutes after BPC 157 application, for frequency after 55 minutes, for PR after 115 minutes and for QTc after 145 minutes. In animals treated with sotalol, an increase in superior sagittal sinus pressure (10 ± 5 mmHg), as well as an increase in portal vein (17 ± 4 mmHg) and inferior caval vein pressures (12 ± 6 mmHg) were noted, along with the decrease in abdominal aortic pressure (53 ± 10 mmHg). These effects were attenuated in BPC treated animals (‐1 ± 1 mmHg for superior sagittal sinus, 7 ± 1 mmHg in portal vein, 5 ± 1 mmHg in inferior caval vein, and 81 ± 7 mmHg in abdominal aorta).In conclusion, BPC 157 attenuated deleterious hemodynamic effects of sotalol while the effects on the ECG parameters were also noted, although not long lasting, supporting the view of BPC‐157 as a rapid‐acting protective agent.

Myocardial Edema Provides a Link Between Pulmonary Arterial Hypertension and Pericardial Effusion.

Myocardial Edema Provides a Link Between Pulmonary Arterial Hypertension and Pericardial Effusion.

Venoconstrictor responses to activation of bradykinin-sensitive pericardial afferents involve the region of the hypothalamic paraventricular nucleus.

Veins are important in the control of venous return, cardiac output, and cardiovascular homeostasis. However, the effector systems modulating venous function remain to be fully elucidated. We demonstrated that activation of bradykinin‐sensitive pericardial afferents elicited systemic venoconstriction. The hypothalamic paraventricular nucleus (PVN) is an important site modulating autonomic outflow to the venous compartment. We tested the hypothesis that the PVN region is involved in the venoconstrictor response to pericardial injection of bradykinin. Rats were anesthetized with urethane/alpha chloralose and instrumented for recording arterial pressure, vena caval pressure, and mean circulatory filling pressure (MCFP), an index of venous tone. The rats were fitted with a pericardial catheter and PVN injector guide tubes. Mean arterial pressure (MAP), heart rate (HR), and MCFP responses to pericardial injection of bradykinin (1, 10 µg/kg) were recorded before and after PVN injection of omega conotoxin GVIA (200 ng/200 nl). Pericardial injection of saline produced no systematic effects on MAP, HR, or MCFP. In contrast, pericardial injection of bradykinin was associated with short latency increases in MAP (16 ± 4 to 18 ± 2 mm Hg) and MCFP 0.35 ± 0.19 to 1.01 ± 0.27 mm Hg. Heart rate responses to pericardial BK were highly variable, but HR was significantly increased (15 ± 9 bpm) at the higher BK dose. Conotoxin injection in the PVN region did not affect baseline values for these variables. However, injection of conotoxin into the area of the PVN largely attenuated the pressor (−1 ± 3 to 6 ± 3 mm Hg), MCFP (−0.19 ± 0.07 to 0.20 ± 0.18 mm Hg), and HR (4 ± 14 bpm) responses to pericardial bradykinin injection. We conclude that the PVN region is involved in the venoconstrictor responses to pericardial bradykinin injection.

Abstract 14301: Investigation of an Injection-Jet Self-Powered Fontan Circulation

Introduction: The Fontan circulation is a fragile system in which imperfections at any one of multiple levels may compromise quality of life. Increased inferior vena caval (IVC) pressure itself may play some role in “Fontan failure”. The Fontan circulation is powered with a high speed injection jet shunt (IJS) drawing flow from the aortic arch, balanced by a fenestration to preserve the ratio of pulmonary flow (Qp) to systemic flow (Qs). The high-velocity jet causes flow entrainment, leading to a significant reduction of upstream pressure. We describe a tightly coupled multi-scale lumped parameter/computational fluids dynamics (LPM-CFD) model to validate this hypothesis. Methods: A synthetic 3D CAD model of the fenestrated total cavopulmonary connection (TCPC) was generated, with average dimensions matching those of a 2-4 yo patient. The prescribed cardiac output is of about 2.3L/min. The detailed 3D pulsatile hemodynamics in the fluid domain are modeled as unsteady, turbulent and incompressible. Blood is assumed to be non-Newtonian. Turbulence is approximated using a large eddy simulation (LES) approach. Potential optimal IJS configurations were determined by with a parametric sweep of several geometric design parameters such as TCPC morphology, shunt diameter and location, and fenestration diameter and location. The effects of the IJS implementation on IVC pressure with a fenestration and systemic oxygen saturation were calculated using a tightly coupled LPM-CFD. Results and Discussion: A set of baseline simulations representing a failing Fontan, with elevated IVC pressure (+17.8mmHg). Enlargement of the fenestration to 7 mm results in a 3 mm Hg IVC pressure drop but also significant reduction in systemic oxygen saturation (assuming a 96% pulmonary venous O2 saturation level). Addition of an IJS (2mm nozzle) to this model preserves the IVC pressure drop of 3.2mmHg but improves systemic oxygen saturation with only a small additional volume load to the ventricle (CO/Qs = 1.2). Conclusions: This study demonstrates the potential salutary effect of the IJS on the Fontan circulation. Further exploration of adjustable anatomic and parameters are needed to further reduce IVC pressure and improve systemic saturation.

In-Vitro Validation of Self-Powered Fontan Circulation for Treatment of Single Ventricle Anomaly

Around 8% of all newborns with a Congenital Heart Defect (CHD) have only a single functioning ventricle. The Fontan operation has served as palliation for this anomaly for decades, but the surgery entails multiple complications, and the survival rate is less than 50% by adulthood. A rapidly testable novel alternative is proposed by creating a bifurcating graft, or Injection Jet Shunt (IJS), used to “entrain” the pulmonary flow and thus provide assistance while reducing the caval pressure. A dynamically scaled Mock Flow Loop (MFL) has been configured to validate this hypothesis. Three IJS nozzles of varying diameters 2, 3, and 4 mm with three aortic anastomosis angles and pulmonary vascular resistance (PVR) reduction have been tested to validate the hypothesis and optimize the caval pressure reduction. The MFL is based on a Lumped-Parameter Model (LPM) of a non-fenestrated Fontan circulation. The best outcome was achieved with the experimental testing of a 3 mm IJS by producing an average caval pressure reduction of more than 5 mmHg while maintaining the clinically acceptable pulmonary flow rate (Qp) to systemic flow rate (Qs) ratio of ~1.5. Furthermore, alteration of the PVR helped in achieving higher caval pressure reduction with the 3 mm IJS at the expense of an increase in Qp/Qs ratio.

Not All Piggybacks Are Equal: A Retrospective Cohort Analysis of Variation in Anhepatic Transcaval Pressure Gradient and Acute Kidney Injury During Liver Transplant.

Complete inferior vena cava clamping in cavalreplacement during livertransplantis associated with substantial physiological derangement and postoperative morbidity. Partial clamping in the piggyback technique may be relatively protective, but evidence is lacking. Having observed substantial variation in transhepatic inferior vena cava pressure gradient with piggyback, we hypothesized that the causative mechanism is the extent of caval clamping rather than the surgical approach. We used internal jugular and femoral catheters to estimate suprahepatic and infrahepatic inferior vena cava pressures during clamping. Pressure gradients were calculated, and distributions were compared by surgical technique. We estimated adjusted odds ratios for pressure gradient on acute kidney injury at 72 hours. In 115 case records, we observed substantial variation in maximum pressure gradient; median values were 18.0 mm Hg(interquartile range, 8.0-25.0 mm Hg) with the piggyback technique and 24.0 mm Hg (interquartile range, 19.5-27.0 mm Hg) with caval replacement. Incidence of acute kidney injury was 25% (29 patients). Pressure gradient was linearly associated with probability of acute kidney injury (odds ratio, 1.06; 95% CI, 1.01-1.13). We report 2 novel findings. (1) Anhepatic inferior vena cavapressuregradient variedsubstantially in individuals undergoing piggyback, and (2) gradient was positively associatedwith early acute kidney injury. We hypothesize that this (unmeasured) variation explains the conflictingfindings ofprevious studies that compared surgical techniques. Also, we propose that caval pressure gradient could be routinely assessed to optimize real-time piggyback clamp position during livertransplant surgery.

A225 INFERIOR VENA CAVA STENOSIS AFTER HEPATIC LOBECTOMY: A RARE CAUSE OF PORTAL HYPERTENSION AND REFRACTORY ASCITES

Abstract Background Inferior vena cava (IVC) stenosis is a rare occurrence in post-liver transplant patients, affecting less than 3% of recipients. IVC stenosis is rarely described in non-transplant patients or considered in the differential of portal hypertension and refractory ascites. Patients with IVC stenosis may experience lower extremity edema, dyspnea, ascites and other signs of portal hypertension. Aims We describe a case of portal hypertension and refractory ascites secondary to IVC stenosis following hepatic lobectomy. Methods Case report. Results We report a 61-year-old woman with a history of diabetes, obesity status post sleeve gastrectomy and solitary neuroendocrine tumor of the right hepatic lobe, adjacent to the porta hepatis with no evidence of metastasis. She underwent a laparoscopic right hepatectomy with wedge resection (&amp;lt;5 cm) in segment 4 to remove the neuroendocrine tumor in 2016. Surgery also included an intraoperative cholangiogram and placement of intra-ductal stent using endoscopic retrograde cholangiopancreatography (ERCP) technology as well as significant adhesiolysis along the IVC, right hepatic vein and biliary tract. In February 2020, the patient was referred to Hepatology for evaluation of new ascites. Imaging did not demonstrate evidence of tumor recurrence or features of cirrhosis but identified a new findings of portal hypertension and moderate ascites. Common causes of chronic liver disease were excluded and hepatic synthetic function was normal. Paracentesis revealed a high serum albumin ascites gradient (SAAG; 20 g/L) and a high ascitic fluid protein (34 g/L). Although these findings were suggestive of cardiac ascites, a 2D echocardiogram was normal. A trans-jugular liver biopsy was attempted in July 2020. The right atrial pressure was 8 mmHg and inferior vena cava (IVC) pressure was 22 mmHg at the level of the liver. Loss of pulsation suggested hemodynamically significant stenosis of the hepatic IVC. The wedged hepatic venous pressure was 3 mmHg and the calculated portal systemic gradient was 4 mmHg. A trans jugular biopsy failed due to unfavourable anatomy. These findings, taken in conjunction with previous results, suggested non-cirrhotic post-hepatic portal hypertension. Subsequent computed tomography imaging confirmed stenosis of the hepatic portion of the IVC and this was felt to be the ultimate cause of the portal hypertension. She has since been referred back to interventional radiology (IR) for consideration of balloon angioplasty dilation of the IVC stenosis as well as additional testing to determine if there is any underlying hepatic fibrosis related to congestive hepatopathy. Conclusions IVC stenosis post hepatic lobectomy is a rare phenomenon described in the literature but warrants high suspicion in cases of refractory ascites. Funding Agencies None

Effects of propofol and sevoflurane on hepatic blood flow: a randomized controlled trial

BackgroundMaintaining adequate perioperative hepatic blood flow (HBF) supply is essential for preservation of postoperative normal liver function. Propofol and sevoflurane affect arterial and portal HBF. Previous studies have suggested that propofol increases total HBF, primarily by increasing portal HBF, while sevoflurane has only minimal effect on total HBF. Primary objective was to compare the effect of propofol (group P) and sevoflurane (group S) on arterial, portal and total HBF and on the caval and portal vein pressure during major abdominal surgery. The study was performed in patients undergoing pancreaticoduodenectomy because - in contrast to hepatic surgical procedures - this is a standardized surgical procedure without potential anticipated severe hemodynamic disturbances, and it allows direct access to the hepatic blood vessels.MethodsPatients were randomized according to the type of anesthetic drug used. For both groups, Bispectral Index (BIS) monitoring was used to monitor depth of anesthesia. All patients received goal-directed hemodynamic therapy (GDHT) guided by the transpulmonary thermodilution technique. Hemodynamic data were measured, recorded and guided by Pulsioflex™. Arterial, portal and total HBF were measured directly, using ultrasound transit time flow measurements (TTFM) and were related to hemodynamic variables.ResultsEighteen patients were included. There was no significant difference between groups in arterial, portal and total HBF. As a result of the GDHT, pre-set hemodynamic targets were obtained in both groups, but MAP was significantly lower in group S (p = 0.01). In order to obtain these pre-set hemodynamic targets, group S necessitated a significantly higher need for vasopressor support (p < 0.01).ConclusionHepatic blood flow was similar under a propofol-based and a sevoflurane-based anesthetic regimen. Related to the application of GDHT, pre-set hemodynamic goals were maintained in both groups, but sevoflurane-anaesthetized patients had a significantly higher need for vasopressor support.Trial registrationStudy protocol number is AGO/2017/002 – EC/2017/0164. EudraCT number is 2017–000071-90.Clin.trail.gov,NCT03772106, Registered 4/12/2018, retrospective registered.

A sensorless physiologic control strategy for continuous flow cavopulmonary circulatory support devices

ObjectiveMechanical circulatory support devices using continuous flow blood pump technologies are currently being developed to provide cavopulmonary support in patients with Fontan circulation. While cavopulmonary support can functionally replace the missing native right ventricle and biventricularize the Fontan circulation, there is a need for the pump to adapt to variable physiologic demands. A constant pump speed limits the ability to provide sufficient physiologic perfusion over a range of physiologic conditions. To address this challenge, a physiologic control algorithm for a Fontan pump was developed. MethodsThe proposed algorithm uses a gain-scheduled, proportional-integral controller that generates a user defined cavopulmonary pressure head (CPPH = pulmonary artery pressure - vena caval pressure), to provide physiologic pressure rise while avoiding suction. The approach uses only intrinsic pump parameters and does not require the use of pressure or flow sensors. Performance and robustness of the sensorless control algorithm was quantified in-silico by simulating the following conditions: (1) Directly measured CPPH with pressure sensors; (2) CPPH estimation using the intrinsic pump measurement of pump speed and extended Kalman filter (EKF); (3) constant speed control algorithm; and (4) rapid four-fold increase in vena caval resistance (VCR) for (1) to (3). ResultsThe results demonstrated that the sensorless control algorithm maintained physiologic perfusion while simultaneously preventing vena caval suction without the need for pressure sensors. Conclusion and significanceThe proposed algorithm was superior to the constant speed control strategy for physiologic perfusion and suction prevention, and warranted further investigation in vitro and in-vivo.

Pentadecapeptide BPC 157 resolves Pringle maneuver in rats, both ischemia and reperfusion.

The Pringle maneuver [portal triad obstruction(PTO)] provides huge disturbances during ischemia and even more thereafter in reperfusion. Contrarily, a possible solution may be stable gastric pentadecapeptide BPC 157, with already documented beneficial effects in ischemia/reperfusion conditions. Recently, BPC 157, as a cytoprotective agent, successfully resolved vessel occlusions in rats (ischemic colitis; deep vein thrombosis, superior anterior pancreaticoduodenal vein; bile duct cirrhosis) through rapid collateral vessel recruitment to circumvent vessel occlusion. Thereby, medication BPC 157 regimens were administered as a single challenge before and during ischemia or, alternatively, at various time points during reperfusion. To introduce BPC 157 therapy against pringle maneuver-damage. In deeply anesthetised rats, the portal triad was clamped up for 30 min. Rats then underwent reperfusion for either 15 min or 24 h. Medication [(10 µg, 10 ng/kg) regimens, administered as a single challenge] picked (a) ischemia, PTO period [at 5 min before (ip) or at 5 or 30 min of ligation time (as a bath to PTO)] or (b) reperfusion, post-PTO period [at 1 or 15 min (bath during surgery) or 24 h (ip) reperfusion-time]. We provided gross, microscopy, malondialdehyde, serum enzymes, electrocardiogram, portal, caval, and aortal pressure, thrombosis and venography assessments. BPC 157 counteracts electrocardiogram disturbances (increased P wave amplitude, S1Q3T3 QRS pattern and tachycardia). Rapidly presented vascular pathway (portal vein-superior mesenteric vein-inferior mesenteric vein-rectal veins-left ileal vein-inferior caval vein) as the adequate shunting immediately affected disturbed haemodynamics. Portal hypertension and severe aortal hypotension during PTO, as well as portal and caval hypertension and mild aortal hypotension in reperfusion and refractory ascites formation were markedly attenuated (during PTO) or completely abrogated (reperfusion); thrombosis in portal vein tributaries and inferior caval vein or hepatic artery was counteracted during portal triad obstruction PTO. Also, counteraction included the whole vicious injurious circle [i.e., lung pathology (severe capillary congestion), liver (dilated central veins and terminal portal venules), intestine (substantial capillary congestion, submucosal oedema, loss of villous architecture), splenomegaly, right heart (picked P wave values)] regularly perpetuated in ischemia and progressed by reperfusion in Pringle rats. BPC 157 resolves pringle maneuver-damage in rats, both for ischemia and reperfusion.

Impact of the superior cavopulmonary anastomosis on cerebral oxygenation.

Patients with univentricular heart disease may undergo a superior cavopulmonary anastomosis, an operative intervention that raises cerebral venous pressure and impedance to cerebral venous return. The ability of infantile cerebral autoregulation to compensate for this is not well understood. We identified all patients undergoing a superior cavopulmonary anastomosis (cases) and compared metrics of cerebral oxygenation upon admission to the ICU with patients following repair of tetralogy of Fallot or arterial switch operation (controls). The primary endpoint was cerebral venous oxyhaemoglobin saturation measured from an internal jugular venous catheter. Other predictor variables included case-control assignment, age, weight, sex, ischemic times, arterial oxyhaemoglobin saturation, mean arterial blood pressure, and superior caval pressure. A total of 151 cases and 350 controls were identified. The first post-operative cerebral venous oxyhaemoglobin saturation was significantly lower following superior cavopulmonary anastomosis than in controls (44 ± 12 versus 59 ± 15%, p < 0.001), as was arterial oxyhaemoglobin saturation (81 ± 9 versus 98 ± 5%, p < 0.001). Cerebral venous oxyhaemoglobin saturation correlated poorly with superior caval pressure in both groups. When estimated by linear mixed effects model, arterial oxyhaemoglobin saturation was the primary determinant of central venous oxyhaemoglobin saturation in both groups (β = 0.79, p = 3 × 10-14); for every 1% point increase in arterial oxyhaemoglobin saturation, there was a 0.79% point increase in venous oxyhaemoglobin saturation. In this model, no other predictors were significant, including superior caval pressure and case-control assignment. Cerebral autoregulation appears to remain intact despite acute imposition of cerebral venous hypertension following superior cavopulmonary anastomosis. Following superior cavopulmonary anastomosis, cerebral venous oxyhaemoglobin saturation is primarily determined by arterial oxyhaemoglobin saturation.

Blunt Aortic / Inferior Vena Cava Injury: Are We Consistently Providing the Same Level of Care?

Major vascular traumatic injuries have a higher pre-hospital and in-hospital mortality rate. The different mechanisms of injury and anatomy of the aorta and inferior vena cava (IVC) make the management a constant challenge to surgeons and clinicians. Blunt traumatic aortic injury (BTAI) can occur at the thoracic or abdominal level, each of which possesses different considerations. Blunt traumatic inferior vena cava injury (BTIVCI) also has important diagnostic challenges since the lesion may not be as evident in the IVC as compared to the aorta, possibly due to lower caval pressures or the ability to self-tamponade from adjacent structures. Endovascular management has significantly increased in the past years, and despite an improvement in mortality, the approach to aortic and IVC injuries is not well standardized. Diagnostic imaging helps to classify the extent of the lesions and guide towards the best therapeutic options for each case. Conservative management, in some cases, has shown to reduce mortality, and close follow-up has proven good outcomes. Future research will provide more evidence to determine the best approach to BTAI and BTIVCI for better long-term outcomes. This article aims to provide an updated review of the current literature regarding diagnosis, classification, and management of BTAI and BTIVCI.

P3590Impact of right ventricular branch slow flow phenomenon post percutaneous coronary intervention for acute coronary syndrome to predict sustained right ventricular dysfunction

Abstract Background Although Right Ventricular dysfunction (RVD) is one of the predictor of poor prognosis, it is believed that ischemic RVD after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) restores quickly. Because right ventricular perfusion has more ischemic preconditioning compared with left ventricle, due to their complex perfusion system. However, little is known about the time courses of RVD after ACS-PCI andtheir prognosis. We evaluated the relationship between right ventricular branch slow flow phenomenon (RVB-SF) post ACS-PCI in right coronary artery (RCA) and RVD at 6–8 months follow-up. Method We retrospectively analyzed consecutive 82 patients who underwent PCI for ACS in proximal or mid portion of RCA from August 2011 to March 2018 in our institution. Finally, both baseline and follow-up data were obtained from 70 patients. We analyzed TIMI frame count (TFC) to confirm the presence of RVB-SF (TFC ≥40 frame) after PCI. We also analyzed right ventricular fractional area change (RVFAC) at baseline and follow-up using echocardiography to detect sustained RVD (RVFAC ≤35%). Result We divided the patients into two groups (RVB-SF: 36 patients, RVB non-SF: 34 patients). Patient clinical characteristics were similar in both groups (sex, age, risk factors, medication, onset to balloon time, left ventricular stroke volume, max creatine kinase). Baseline RVFAC and follow-up RVFAC was significantly smaller in RVB-SF than in RVB non-SF, respectively. (27.1±1.7% vs. 38.3±1.8%, 31.4±1.0% vs. 48.7±1.1%, P&lt;0.0001). However, ΔRVFAC (follow-up RVFAC – baseline RVFAC) was similar between groups. The size of inferior vena cava and systolic pulmonary artery pressure at follow-up were similar in both groups (12.1±0.6 mm vs. 11.7±0.7 mm, P=0.67, 25.7±1.5 mmHg vs. 25.2±1.5 mmHg, P=0.82). In RVB non-SF, 10 patients (29.4%) were diagnosed clinical RVAMI. However, follow-up RVFAC were similar and preserved in both groups (RVAMI: 48.1±1.3%, non-RVAMI: 49.9±1.9%, P=0.85). In RVB-SF, 19 patients (52.7%) were diagnosed clinical RVAMI. Follow-up RVFAC did not improved significantly in both groups (RVAMI: 30.4±1.4% vs. non-RVAMI: 32.6±1.5%, P=0.70). Multivariate analysis showed RVB-SF was the only independent predictor of sustained RVD at 6–8 months follow-up after ACS-PCI. Conclusion RVB-SF findings after ACS-PCI for RCA could predict sustained RVD at mid-term follow-up, which may indicate future prolonged RVD.

Patient-Specific Multiscale Modeling of the Assisted Bidirectional Glenn

First-stage palliation of neonates with single-ventricle physiology is associated with poor outcomes and challenging clinical management. Prior computational modeling and invitro experiments introduced the assisted bidirectional Glenn (ABG), which increased pulmonary flow and oxygenation over the bidirectional Glenn (BDG) and the systemic-to-pulmonary shunt in idealized models. In this study, we demonstrate that the ABG achieves similar performance in patient-specific models and assess the influence of varying shunt geometry. In a small cohort of single-ventricle prestage 2 patients, we constructed three-dimensional in silico models and tuned lumped parameter networks to match clinical measurements. Each model was modified to produce virtual BDG and ABG surgeries. We simulated the hemodynamics of the stage 1 procedure, BDG, and ABG by using multiscale computational modeling, coupling a finite-element flow solver to the lumped parameter network. Two levels of pulmonary vascular resistances (PVRs) were investigated: baseline (low) PVR of the patients and doubled (high) PVR. The shunt nozzle diameter, anastomosis location, and shape were also manipulated. The ABG increased the pulmonary flow rate and pressure by 15% to 20%, which was accompanied by a rise in superior vena caval pressure (2 to 3 mm Hg) at both PVR values. Pulmonary flow rate and superior vena caval pressures were most sensitive to the shunt nozzle diameter. Patient-specific ABG performance was similar to prior idealized simulations and experiments, with good performance at lower PVR values in the range of measured clinical data. Larger shunt outlet diameters and lower PVR led to improved ABG performance.

Optimization of the Assisted Bidirectional Glenn Procedure for First Stage Single Ventricle Repair.

First-stage single-ventricle palliation is challenging to manage, and significant interstage morbidity and mortality remain. Prior computational and in vitro studies of the assisted bidirectional Glenn (ABG), a novel first-stage procedure that has shown potential for early conversion to a more stable augmented Glenn physiology, demonstrated increased pulmonary flow and oxygen delivery while decreasing cardiac work, as compared to conventional stage-1 alternatives. This study aims to identify optimal shunt designs for the ABG to improve pulmonary flow while maintaining or decreasing superior vena caval (SVC) pressure. A representative three-dimensional model of a neonatal bidirectional Glenn (BDG) was created, with a shunt connecting the innominate artery to the SVC. The shunt design was studied as a six-parameter constrained shape optimization problem. We simulated hemodynamics for each candidate designs using a multiscale finite element flow solver and compared performance against designs with taper-less shunts, the standalone BDG, and a simplified control volume model. Three values of pulmonary vascular resistance (PVR) of 2.3, 4.3, and 7.1 WUm2 were studied. Increases in pulmonary flow were generally accompanied by increases in SVC pressure, except at low PVR (2.3 WUm2), where the optimal shunt geometry achieved a 13% increase in pulmonary flow without incurring any increase in SVC pressure. Shunt outlet area was the most influential design parameter, while others had minimal effect. Assisted bidirectional Glenn performance is sensitive to PVR and shunt outlet diameter. An increase in pulmonary flow without a corresponding increase in SVC pressure is possible only when PVR is low.