Transpulmonary Blood Flow Research Articles

Cochlear Implantation with Fontan Circulation: A Rare Case of Non-Cardiac Pediatric Surgery

Background: Fontan circulation is a cardiac circulation following the Fontan procedure in patients with a single ventricle congenital heart defect. This circulation depends on the difference in pressure between pulmonary capillaries and central venous pressure to achieve optimal cardiac output. This case report aims to discuss intraoperative anesthesia management in a patient with Fontan circulation undergoing a non-cardiac surgical operation.
 Case presentation: The patient is a 7-year-old male with a history of congenital heart disease who has undergone the Fontan circulation procedure and is now undergoing Cochlear implantation surgery. The patient was managed with general anesthesia - endotracheal intubation and controlled ventilation during the operation, following the principle of minimizing intrathoracic positive pressure, low PEEP, and low tidal volume with a target peripheral saturation > 95%. Cardiac output monitoring during the intraoperative period is done using intra-arterial blood pressure. After 5 hours of surgery, the patient was extubated with stable hemodynamics. 
 Conclusion: The primary goal of intraoperative anesthesia management in patients with Fontan circulation is to maintain an optimal transpulmonary gradient by ensuring optimal transpulmonary blood flow, thus preserving cardiac output.

The physiology of extracorporeal membrane oxygenation: The Fick principle.

Extracorporeal membrane oxygenation (ECMO) can be delivered in veno-arterial (VA) and veno-venous (VV) configurations based on the cannulation strategy. VA and VV ECMO are delivered primarily for haemodynamic and respiratory support in patients with severe heart and lung failure, respectively. The Fick principle describes the relationship between blood flow and oxygen consumption - key parameters in the physiological management of extracorporeal support. This review will discuss the application of the Fick principle in: (i) recirculation in VV ECMO; (ii) the quantification of oxygen delivery (DO2) in VV ECMO and (iii) the quantification of transpulmonary blood flow and systemic arterial oxygen saturation in VA ECMO.

The pulmonary vascular bed in patients with functionally univentricular physiology and a Fontan circulation.

Fontan palliation represents one of the most remarkable surgical advances in the management of individuals born with functionally univentricular physiology. The operation secures adult survival for all but a few with unfavourable anatomy and/or physiology. Inherent to the physiology is passive transpulmonary blood flow, which produces a vulnerability to adequate filling of the systemic ventricle at rest and during exertion. Similarly, the upstream effects of passive flow in the lungs are venous congestion and venous hypertension, especially marked during physical activity. The pulmonary vascular bed has emerged as a defining character on the stage of Fontan circulatory behaviour and clinical outcomes. Its pharmacologic regulation and anatomic rehabilitation therefore seem important strategic therapeutic targets. This review seeks to delineate the important aspects of pulmonary artery development and maturation in functionally univentricular physiology patients, pulmonary artery biology, pulmonary vascular reserve with exercise, and pulmonary artery morphologic and pharmacologic rehabilitation.

Incremental Value of ePLAR-The Echocardiographic Pulmonary to Left Atrial Ratio in the Assessment of Sub-Massive Pulmonary Emboli.

Background: Acute pulmonary embolism (PE) is characterized hemodynamically by abrupt obstruction in trans-pulmonary blood flow. The echocardiographic Pulmonary to Left Atrial ratio (ePLAR, tricuspid regurgitation Vmax/mitral E/e’) has been validated as a non-invasive surrogate for trans-pulmonary gradient (TPG) that accurately differentiates pre-capillary from post-capillary chronic pulmonary hypertension. This study assessed ePLAR as an incremental echocardiographic assessment tool compared with traditional measures of right ventricular pressure and function. Methods: In total, 110 (57.4 ± 17.6 years) patients with confirmed sub-massive pulmonary emboli with contemporaneous echocardiograms (0.3 ± 0.9 days) were compared with 110 age-matched controls (AMC). Results: Tricuspid velocities were higher than AMC (2.6 ± 0.6 m/s vs. 2.4 ± 0.3 m/s, p < 0.05), although still consistent with “normal” right ventricular systolic pressures (34.2 ± 13.5 mmHg vs. 25 ± 5.3 mmHg, p < 0.05) with lower mitral E/e’ values (8.2 ± 3.8 vs. 10.8 ± 5.1, p < 0.05). ePLAR values were higher than AMC (0.36 ± 0.14 m/s vs. 0.26 ± 0.10, p < 0.05) suggesting significantly elevated TPG. Detection of abnormal echocardiographic findings increased from 29% (TRVmax ≥ 2.9 m/s) and 32% (reduced tricuspid annular plane systolic excursion) to 70% with ePLAR ≥ 0.3 m/s. Conclusions: Raised ePLAR values in acute sub-massive pulmonary embolism suggest elevated trans-pulmonary gradients even in the absence of acutely increased pulmonary artery pressures. ePLAR dramatically increases the sensitivity of echocardiography for detection of hemodynamic perturbations in sub-massive pulmonary embolism patients, which may offer clinical utility in diagnosis and management.

Inhaled nitric oxide improves transpulmonary blood flow and clinical outcomes after prolonged cardiac arrest: a large animal study.

IntroductionThe probability to achieve a return of spontaneous circulation (ROSC) after cardiac arrest can be improved by optimizing circulation during cardiopulomonary resuscitation using a percutaneous left ventricular assist device (iCPR). Inhaled nitric oxide may facilitate transpulmonary blood flow during iCPR and may therefore improve organ perfusion and outcome.MethodsVentricular fibrillation was electrically induced in 20 anesthetized male pigs. Animals were left untreated for 10 minutes before iCPR was attempted. Subjects received either 20 ppm of inhaled nitric oxide (iNO, n = 10) or 0 ppm iNO (Control, n = 10), simultaneously started with iCPR until 5 hours following ROSC. Animals were weaned from the respirator and followed up for five days using overall performance categories (OPC) and a spatial memory task. On day six, all animals were anesthetized again, and brains were harvested for neurohistopathologic evaluation.ResultsAll animals in both groups achieved ROSC. Administration of iNO markedly increased iCPR flow during CPR (iNO: 1.81 ± 0.30 vs Control: 1.64 ± 0.51 L/min, p < 0.001), leading to significantly higher coronary perfusion pressure (CPP) during the 6 minutes of CPR (25 ± 13 vs 16 ± 6 mmHg, p = 0.002). iNO-treated animals showed significantly lower S-100 serum levels thirty minutes post ROSC (0.26 ± 0.09 vs 0.38 ± 0.15 ng/mL, p = 0.048), as well as lower blood glucose levels 120–360 minutes following ROSC. Lower S-100 serum levels were reflected by superior clinical outcome of iNO-treated animals as estimated with OPC (3 ± 2 vs. 5 ± 1, p = 0.036 on days 3 to 5). Three out of ten iNO-treated, but none of the Control animals were able to successfully participate in the spatial memory task. Neurohistopathological examination of vulnerable cerebral structures revealed a trend towards less cerebral lesions in neocortex, archicortex, and striatum in iNO-treated animals compared to Controls.ConclusionsIn pigs resuscitated with mechanically-assisted CPR from prolonged cardiac arrest, the administration of 20 ppm iNO during and following iCPR improved transpulmonary blood flow, leading to improved clinical neurological outcomes.

Abstract 12202: Inhaled Nitric Oxide Improves Artificial Circulation and Clinical Outcomes After Prolonged Cardiac Arrest

Introduction: Primary survival after cardiac arrest can be improved by optimizing circulation during CPR when using a minimal invasive left ventricular assist device (iCPR). Hypothesis: Inhaled nitric oxide may facilitate transpulmonary bloodflow during iCPR and thereby improve the functional outcome following cardiac arrest. Methods: Ventricular fibrillation (VF) was electrically induced in 20 anesthetized male pigs. Animals were left untreated for 10 minutes before iCPR was attempted. Subjects received either 20ppm of inhaled nitric oxide (iNO, n = 10) or 0ppm iNO (Control, n = 10), simultaneously started with iCPR until 5 hours following return of spontaneous circulation (ROSC). Animals were weaned from the respirator and followed up for five days using overall performance categories (OPC) and a spatial memory task. On day six, all animals were anesthetized again, and brains harvested for neurohistopathologic evaluation. Results: All animals in both groups achieved ROSC. iNO treated animals reached significantly higher iCPR flow during CPR (1.81 ± 0.30 L/min compared to 1.64 ± 0.51, p&lt;0.001), leading to significantly higher coronary perfusion pressure (CPP) values during the 6 minutes of CPR (25 ± 13 vs. 16 ± 6 mmHg, p = 0.002). iNO animals showed significantly lower S-100 serum levels thirty minutes post ROSC (0.26 ± 0.09 vs. 0.38 ± 0.15 ng/mL, p = 0.048), as well as lower blood glucose values 120-360 minutes following ROSC. Lower S-100 serum levels were reflected by superior clinical outcome of iNO treated animals as estimated with OPC (3 ± 2 vs. 5 ± 1, p = 0.036 on days 3 to 5). While n = 3 iNO treated animals were able to successfully participate in the spatial memory task, none of the controls were able to do so. Neurohistopathological examination of cerebral structures prone to ischemia-reperfusion injury revealed a trend towards less cerebral lesions in Neocortex, Archicortex, and Striatum when animals had been treated with iNO. Conclusions: In a model of prolonged cardiac arrest, the administration of 20ppm iNO during and following iCPR improved transpulmonary bloodflow and mitigated post-aggression metabolism, indicated by lower serum glucose levels. These effects translated into improved clinical outcomes in iNO treated animals.

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Rationale and design of a trial on the role of bosentan in Fontan patients: Improvement of exercise capacity?

Background The Fontan circulation is a palliative procedure performed in patients with complex congenital heart disease (CHD), making transpulmonary blood flow dependent on the systemic venous pressure. In a Fontan circulation a low pulmonary vascular resistance (PVR) is crucial, as is epitomized by the observation that a high PVR is a strong predictor of mortality. Long-term follow-up has shown that PVR may rise many years after the Fontan procedure has been performed, possibly due to micro-emboli from a dilated right atrium or from the venous system. Other mechanisms of increased PVR might be aging, obstructed airways caused by lymphatic dysfunction, lack of pulsatile pulmonary flow causing a release of endothelium-derived vasoactive molecules, and prolonged overexpression of vasoconstrictors such as endothelin-1. Mean plasma level of endothelin-1 has been shown to be significantly higher in Fontan patients compared to healthy controls. In patients with pulmonary arterial hypertension (PAH), therapy with bosentan, an endothelin-1 receptor antagonist, has demonstrated to improve exercise capacity and to reduce the elevated PVR. In addition, reduction of PVR is shown early and late after the Fontan procedure on treatment with exogenous NO, another advanced PAH therapy. However, the long term effect of reducing the PVR by bosentan treatment on exercise capacity in Fontan patients is still unknown. Methods We designed a prospective, multicenter, randomized open label trial to study the effect of bosentan in Fontan patients. The primary endpoint will be the change in maximum exercise capacity (peak V'O2). Conclusion We hypothesize that treatment with bosentan, an endothelin-1 receptor antagonist, improves maximum exercise capacity and functional capacity in adult Fontan patients.

Mechanisms of systemic adaptation to univentricular Fontan conversion

After univentricular Fontan conversion, systemic venous pressure serves as the sole driving force for transpulmonary blood flow. Consequently, systemic venous return is markedly altered and ventricular filling is subnormal. The mechanisms and time course of systemic adaptation to Fontan conversion are incompletely understood. We hypothesized that acute elevation in systemic venous pressure induces an adaptive response similar to conversion to a univentricular Fontan circulation. Adjustable vessel occluders were placed around the superior and inferior vena cavae in juvenile sheep. After 1-week recovery, occluders were tightened to acutely increase and maintain systemic venous pressure at 15 mm Hg (n = 6), simulating 1-stage Fontan conversion. Control animals (n = 4) received identical surgery, but venous pressure was not manipulated. Cardiac index decreased significantly (3.9 ± 1.0 mL/min/m(2) to 2.7 ± 0.7 mL/min/m(2), P < .001) and then normalized to control at 2 weeks. Circulating blood volume increased (100 ± 9.4 mL/kg vs 85.5 ± 8.4 mL/kg, P = .034) as a persistent response. Cardiac reserve improved and was not different from control by week 3. Resting heart rate decreased in both groups. Oxygen extraction (arteriovenous oxygen difference) and neurohormonal mediators increased transiently and then normalized by week 2. Adaptation to global elevation in systemic venous pressure to Fontan levels is complete within 2 weeks. Increased blood volume and reduced heart rate are persistent responses. Increased oxygen extraction and neurohormonal up-regulation are temporary responses that normalize with recovery of cardiac output. With improved physiologic understanding of systemic adaptation to Fontan conversion, approaches to single-ventricle palliation can be more objectively assessed and optimized.

Vasodilation increases pulse pressure variation, mimicking hypovolemic status in rabbits

OBJECTIVETo test the hypothesis that pulse pressure respiratory variation (PPV) amplification, observed in hypovolemia, can also be observed during sodium nitroprusside (SNP)-induced vasodilation.INTRODUCTIONPPV is largely used for early identification of cardiac responsiveness, especially when hypovolemia is suspected. PPV results from respiratory variation in transpulmonary blood flow and reflects the left ventricular preload variations during respiratory cycles. Any factor that decreases left ventricular preload can be associated with PPV amplification, as seen in hypovolemia.METHODSTen anesthetized and mechanically ventilated rabbits underwent progressive hypotension by either controlled hemorrhage (Group 1) or intravenous SNP infusion (Group 2). Animals in Group 1 (n = 5) had graded hemorrhage induced at 10% steps until 50% of the total volume was bled. Mean arterial pressure (MAP) steps were registered and assumed as pressure targets to be reached in Group 2. Group 2 (n = 5) was subjected to a progressive SNP infusion to reach similar pressure targets as those defined in Group 1. Heart rate (HR), systolic pressure variation (SPV) and PPV were measured at each MAP step, and the values were compared between the groups.RESULTSSPV and PPV were similar between the experimental models in all steps (p > 0.16). SPV increased earlier in Group 2.CONCLUSIONBoth pharmacologic vasodilation and graded hemorrhage induced PPV amplification similar to that observed in hypovolemia, reinforcing the idea that amplified arterial pressure variation does not necessarily represent hypovolemic status but rather potential cardiovascular responsiveness to fluid infusion.

Comparison of Patterns of Pulmonary Venous Blood Flow in the Functional Single Ventricle Heart After Operative Aortopulmonary Shunt Versus Superior Cavopulmonary Shunt

In this study we investigated the patterns of pulmonary venous flow in children with functional single ventricles to obtain a better understanding of the determinants of transpulmonary blood flow. Sixty-eight patients with functional single ventricles and aortopulmonary shunt (n = 34, group I), or superior cavopulmonary connection (n = 34, group II) underwent transesophageal Doppler echocardiographic assessment of flow in the left upper pulmonary vein before undergoing the next stage of surgery. Twelve patients from group II also underwent simultaneous evaluation of superior vena caval flow. Biphasic forward pulmonary venous flow was noted in 62 patients in sinus rhythm (S wave in systole, D wave in diastole); in 6 patients with junctional rhythm, significant early systolic reversal of flow was present. Both the S- and D-wave velocity-time integrals (VTI) were greater in group I than in group II (S VTI 9.9 ± 4.2 vs 8.0 ± 2.6, p = 0.02; D VTI 8.0 ± 3.5 vs 4.2 ± 2.6, p <0.001). In both groups, pulmonary venous flow was predominantly systolic; however, the proportion of flow during ventricular systole was significantly greater in group II than in group I (S VTI/D VTI group II: 2.4 ± 1.5; group I 1.4 ± 0.5, p = 0.001; percent systolic fraction of pulmonary venous flow group II = 67%, group I = 56%, p <0.001). Analysis of superior vena caval flow in group II revealed a single predominant wave with onset at early systole and peak in late systole at a mean of 150 ms after the pulmonary venous S-wave peak. Our data suggest that ventricular systole (i.e., atrial relaxation, atrioventricular valve descent) asserts great influence on transpulmonary blood flow in the functional single ventricle.

Major intrahepatic venovenous fistulas after a modified Fontan operation

After the Fontan operation, systemic venous hypertension drives transpulmonary blood flow. Owing to this physiology, there is a significant incidence of effusions, splanchnic congestion, and generalized edema. To attentuate the effusive problems, partial exclusion of the hepatic veins has been recently practiced by Jacobs and Norwood. This report concerns a patient we recently treated for profound progressive cyanosis due to an acquired intrahepatic venovenous shunt after a Fontan operation with partial hepatic vein exclusion.

Intracardiac blood flow velocity waveforms in normal fetuses in utero

Sixty-five continuous-wave Doppler ultrasonographic examinations were performed on 57 normal fetuses at 16 to 40 weeks of gestation. Maximal velocities of transmitral, transtricuspid, transaortic and transpulmonary blood flow velocity waveforms were assessed. Transmitral maximal velocity, transtricuspid maximal velocity, transaortic maximal velocity and transpulmonary maximal velocity correlated well with gestational age. The ratio of transtricuspid maximal velocity/transmitral maximal velocity was at least 1 in 44 of 45 fetuses (97.8%). In the ratio of transpulmonary maximal velocity/transaortic maximal velocity, the characteristic change was not evident. Therefore, continuous-wave Doppler ultrasonographic measurement of fetal intracardlac blood flow velocity waveforms in utero can aid in analyzing the physiologic circulatory hemodynamics.

Myoventriculoplasty and neoventricle myograft cardiac augmentation to establish pulmonary blood flow: Preliminary observations and feasibility studies

In 10 dogs, a latissimus dorsi muscle (myograft) was neuroelectrically stimulated at 120 cycles/min for as long as 80 days. The higher thresholds and multiple lead penetrations required of direct muscle stimulation for muscle conditioning were avoided. Vascular delay and protective wrapping of the myograft in four dogs resulted in rapid seroma and fibrous sheath formation, which precluded further study. Of the six other myografts that were stimulated, two were used as functional right ventricular myoventriculoplasties and four were employed as neoventricle myografts with inflow and outflow valved conduits that were used to provide total pulmonary blood flow. Myoventriculoplasty produced functional enlargement of the right ventricle with synchronously contractile muscle. Neoventricles provided hemodynamically stable total pulmonary blood flow for as long as 20 hours, until internal chamber thrombus formed. Transpulmonary blood pressure generation by the neoventricle was found to be programmable up to physiologic systemic pressures by modulation of chamber preload and burst stimulation frequency at 50 msec intervals, delivered 120 times per minute. Synchronization capabilities for implantable burst pulse generators would further improve the efficacy of these myograft techniques designed to augment or supplant ventricular function, particularly to provide transpulmonary blood flow at programmable pressures.

Intermittent positive pressure and extrathoracic assisted breathing in hypovolemia. Comparative hemodynamic effects.

A comparative analysis of the cardiopulmonary effects of intermittent positive pressure breathing (IPPB) and extrathoracic assisted breathing (ETAB) has been performed in closed-chest anesthetized animals subjected to sublethal acute hemorrhage. Equal inspiratory times and rates were maintained at high tidal volumes with a prolonged inspiratory phase. Significant suppression of cardiac output occurred in all trials, with slightly less suppression accompanying ETAB. Respiratory phase analysis of central venous and pulmonary arterial pressures suggests that impedance to transpulmonary blood flow occurred with IPPB primarily during inspiration and with ETAB during expiration, although of lesser degree. The greater interference of IPPB with cardiac output was largely due to its detrimental phase being twice as long as that of ETAB.