For the last two decades heart disease has been the highest single cause of death for the human population. With an alarming number of patients requiring heart transplant, and donations not able to satisfy the demand, treatment looks to mechanical alternatives. Rotary Ventricular Assist Devices, VADs, are miniature pumps which can be implanted alongside the heart to assist its pumping function. These constant flow devices are smaller, more efficient and promise a longer operational life than more traditional pulsatile VADs. The development of rotary VADs has focused on single pumps assisting the left ventricle only to supply blood for the body. In many patients however, failure of both ventricles demands that an additional pulsatile device be used to support the failing right ventricle. This condition renders them hospital bound while they wait for an unlikely heart donation. Reported attempts to use two rotary pumps to support both ventricles concurrently have warned of inherent haemodynamic instability. Poor balancing of the pumps’ flow rates quickly leads to vascular congestion increasing the risk of oedema and ventricular ‘suckdown’ occluding the inlet to the pump. This thesis introduces a novel Bi-Ventricular Assist Device (BiVAD) configuration where the pump outputs are passively balanced by vascular pressure. The BiVAD consists of two rotary pumps straddling the mechanical passive controller. Fluctuations in vascular pressure induce small deflections within both pumps adjusting their outputs allowing them to maintain arterial pressure. To optimise the passive controller’s interaction with the circulation, the controller’s dynamic response is optimised with a spring, mass, damper arrangement. This two part study presents a comprehensive assessment of the prototype’s ‘viability’ as a support device. Its ‘viability’ was considered based on its sensitivity to pathogenic haemodynamics and the ability of the passive response to maintain healthy circulation. The first part of the study is an experimental investigation where a prototype device was designed and built, and then tested in a pulsatile mock circulation loop. The BiVAD was subjected to a range of haemodynamic imbalances as well as a dynamic analysis to assess the functionality of the mechanical damper. The second part introduces the development of a numerical program to simulate human circulation supported by the passively controlled BiVAD. Both investigations showed that the prototype was able to mimic the native baroreceptor response. Simulating hypertension, poor flow balancing and subsequent ventricular failure during BiVAD support allowed the passive controller’s response to be assessed. Triggered by the resulting pressure imbalance, the controller responded by passively adjusting the VAD outputs in order to maintain healthy arterial pressures. This baroreceptor-like response demonstrated the inherent stability of the auto regulating BiVAD prototype. Simulating pulmonary hypertension in the more observable numerical model, however, revealed a serious issue with the passive response. The subsequent decrease in venous return into the left heart went unnoticed by the passive controller. Meanwhile the coupled nature of the passive response not only decreased RVAD output to reduce pulmonary arterial pressure, but it also increased LVAD output. Consequently, the LVAD increased fluid evacuation from the left ventricle, LV, and so actually accelerated the onset of LV collapse. It was concluded that despite the inherently stable baroreceptor-like response of the passive controller, its lack of sensitivity to venous return made it unviable in its present configuration. The study revealed a number of other important findings. Perhaps the most significant was that the reduced pulse experienced during constant flow support unbalanced the ratio of effective resistances of both vascular circuits. Even during steady rotary support therefore, the resulting ventricle volume imbalance increased the likelihood of suckdown. Additionally, mechanical damping of the passive controller’s response successfully filtered out pressure fluctuations from residual ventricular function. Finally, the importance of recognising inertial contributions to blood flow in the atria and ventricles in a numerical simulation were highlighted. This thesis documents the first attempt to create a fully auto regulated rotary cardiac assist device. Initial results encourage development of an inlet configuration sensitive to low flow such as collapsible inlet cannulae. Combining this with the existing baroreceptor-like response of the passive controller will render a highly stable passively controlled BiVAD configuration. The prototype controller’s passive interaction with the vasculature is a significant step towards a highly stable new generation of artificial heart.

Context: Scimitar syndrome is a congenital anomaly of pulmonary venous return where right pulmonary artery drains into right side other heart, instead of the left side, causing pulmonary hypertension resulting in shortness of breath, recurrent lower respiratory tract infections, chest pain, and fatigue. Early diagnosis and surgical intervention would correct this congenital anomaly reducing morbidity and complications in otherwise healthy young patients. Case Report: We present a case of an 18-year-old female who presented with exertional shortness of breath, fatigue, and recurrent lower respiratory tract infections. She had unremarkable physical examination but chest x-ray showed an abnormal opacity next to right heart border. Computed tomography (CT) chest was performed that showed possible scimitar syndrome. Transesophageal echocardiogram (TEE) and right heart catheterization (RHC) confirmed the diagnosis. Conclusion: Scimitar syndrome is a very rare congenital anomaly of pulmonary venous return. It is usually diagnosed in early childhood but the diagnosis may be delayed until later in adulthood. The consequences are pulmonary hypertension, right-sided heart failure, and frequent pulmonary infections resulting in increased morbidity, mortality, and frequent doctor visits for otherwise healthy young patients.

Background: In morbidly obese individuals (MO) cardiorespiratory comorbidities and body habitus challenge the perioperative management of anesthesia. To implement safe and reproducible routines for anesthesia and fluid therapy is the cornerstone in order to minimize anesthesia-related complications and to meet individual variability in rehydration needs. Methods: Paper I: Impact of rapid-weight-loss preparation prior to bariatric surgery was investigated. Prevalence of preoperative dehydration and cardiac function were assessed with transthoracic echocardiography (TTE). Paper II: The anesthetic technique for rapid sequence induction (RSI) in MO based on a combination of volatile and i.v. anesthetics was developed. Pre- and post-induction oxygenation, blood pressure levels and feasibility of the method was evaluated. Paper III: The preoperative ideal body weight based rehydration regime was evaluated by TTE. Paper IV: Need of rehydration during bariatric surgery was evaluated by comparing conventional monitoring to a more advanced approach (i.e. preoperative TTE and arterial pulse wave analysis). Results: Rapid-weight-loss preparation prior to bariatric surgery may expose MO to dehydration. TTE was shown to be a robust modality for preoperative screening of the level of venous return, assessment of filling pressures and biventricular function of the heart in MO. The combination of sevoflurane, propofol, alfentanil and suxamethonium was demonstrated to be a safe method for RSI regardless of BMI. The preoperative rehydration regime implemented by colloids 6 ml/kg IBW was an adequate treatment to obtain euvolemia. In addition, preoperative rehydration seems to increase hemodynamic stability during intravenous induction of anesthesia and even intraoperatively. Conclusion: This thesis describes a safe and comprehensive perioperative management of morbidly obese individuals scheduled for bariatric surgery. Hemodynamic and respiratory stability can be achieved by implementation of strict and proven methods of anesthesia and fluid therapy. Much focus should be placed on feasible monitoring and preoperative optimization in morbidly obese individuals for increased perioperative safety.

In order to address the long-term complications that arise from poor venous return, a hallmark of the Fontan physiology, we assessed the feasibility of a non-invasive, home therapy that will improve the health of the patient during the heart transplant waiting period and ameliorate the quality of life. In order to achieve this goal we tested a device that applies pressure to the lower extremities of the body (legs and abdomen) in a pulsating fashion with the goal of augmenting systemic blood flow to the pulmonary arteries. This treatment will enhance flow from the great veins and through the lungs and serve as adjunctive clinical treatment of single ventricle physiology. The specific aim of this study was to show improvements in cardiorespiratory measurements after applying external pressure as a proxy for improved health in the Fontan patient. Various studies have shown the impaired exercise capacity of post-operative Fontan patients, but very little data exists focusing on a period much later after the surgery. Our results among the two subjects completed so far have shown a moderately beneficial improvement in exercise capacity after the compression therapy. Subjects performed a treadmill exercise stress test at VCU that was followed by six days of applied external pressure treatment and finished with a final post-treatment stress test. Cardiorespiratory data was collected and analyzed for improvements from base level. Overall an improvement in exercise duration time, VO2 peak, ventilatory threshold, and OUES was observed, with only VE / VCO2 slope having mixed results. Both subjects seem to be relatively healthy Fontan patients, as indicated by their VO2 peak, VE/VCO2 slope and OUES. As a result, benefits of treatment may vary among a cohort of Fontan patients with poor health condition; a failing Fontan physiology for instance. The improvement in exercise capacity suggests that this therapy could be very beneficial to Fontan patients. These results warrants follow up studies to explore the extent of the clinical benefits of compression treatment among the Fontan population.

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