Pulmonary Flow Resistive Device
Reported By:
Taya Furmanski and Albert Attia
Department of Biomedical Engineering
Vanderbilt University
April 22, 2003
Advisor: Dr. Thomas Doyle
Associate Professor of Pediatrics and Director of Pediatric Catheterization Laboratory, Division of Pediatric Cardiology, Vanderbilt University Medical Center
Instructor: Dr. Paul King
Associate Professor of Biomedical and Mechanical Engineering, Vanderbilt University School of Engineering
TABLE OF CONTENTS
1. ABSTRACT…………………………………………………………………………… 3
2. INTRODUCTION
2.1. HYPOPLASTIC LEFT HEART SYNDROME
2.1.1. DEFINITION……………………………………………………………... 4
2.1.2. ANATOMY AND PHYSIOLOGY………………………………………. 4
2.1.3. CAUSE…………………………………………………………………… 6
2.1.4. CLINICAL EPIDEMIOLOGY…………………………………………… 6
2.2 CURRENT TREATMENTS
2.2.1. DRUG TREATMENTS………………………………………………….. 7
2.2.2. RECONSTRUCTIVE SURGERY……………………………………… 7
2.2.3. HEART TRANSPLANT………………………………………………… 8
2.3. DESIGN GOALS……………………………………………………………….. 8
3. METHODOLOGY
3.1. TIMELINE……………………………………………………………………….. 9
3.2. DESIGN AND PROTOTYPE
3.2.1. BACKGROUND…………………………………………………………. 10
3.3. TESTING
3.3.1. METHODS………………………………………………………………. 11
4. RESULTS
4.1. DESIGN
4.1.1. CONE DESIGN…………………………………………………………. 12
4.1.2. OTHER DESIGNS……………………………………………………… 14
4.2. SAFETY ANALYSIS…………………………………………………………… 15
4.3. EC0NOMIC ANALYSIS……………………………………………………….. 17
5. CONCLUSIONS……………………………………………………………………… 18
6. RECOMMENDATIONS……………………………………………………………… 19
7. REFERENCES……………………………………………………………………….. 21
APPENDIX
A. SCHEMATIC OF HEART WITH AND WITHOUT DEVICE
B. DESIGNSAFE REPORT
C. INNOVATION WORKBENCH RESULTS
1. ABSTRACT
Hypoplastic Left Heart Syndrome (HLHS) is a congenital disease that results in the underdevelopment of the left side of the heart. The embryologic cause of HLHS is not fully known; however it is thought to most likely result from either a reduction of left ventricular inflow or left ventricular outflow during development. Approximately 1440 babies are born each year in the United States with HLHS. Current treatments include reconstructive heart surgery and heart transplantation. The goal of our design is to eliminate the first two steps of reconstructive surgery while at the same time ensuring adequate systemic blood flow is achieved. Because the relative ratio of pulmonary to systemic blood flow depends on the balance between pulmonary and systemic vascular resistances, our device focuses on this relationship for treatment solutions. Thus, we have proposed a device that will increase the pulmonary resistance, thereby increasing the flow of blood through the ductus arteriosis and increasing oxygenated systemic blood flow. We began research and brainstorming HLHS in December of 2002. The completion date for this device is April 22, 2003. After exploring other options and presenting them to Dr. Doyle, we decided that the device should have a conical shape. Among the reasons for our conclusion were the effectiveness of the device in impeding flow, the ease at which it could be placed in the arteries, and the low health risks it provided for the patient. It was shown that the device decreased flow; however, the pressure drop across the device needed to be measured and this requires an in vivo model. In addition, animal testing needs to be conducted to test the effectiveness of the device. Afterward, human clinical trials would be required, with the approval of the FDA and the IRB. We believe these are the steps the next group should pursue.
2. INTRODUCTION
2.1 HYPOPLASTIC LEFT HEART SYNDROME
2.1.1 DEFINITION
Hypoplastic Left Heart Syndrome (HLHS) is a congenital disease that results in the underdevelopment of the left side of the heart. With hypoplasia being defined as the underdevelopment of a tissue or organ, this disease extends to the cardiac structures of the left atrium and ventricle, the mitral valve, the aortic valve, and the aorta [4].
2.1.2 ANATOMY AND PHYSIOLOGY
A normal heart functions with both sides of the heart simultaneously pumping equal amounts of blood. The right ventricle is responsible for receiving oxygen-poor blood from the body and pumping it to the lungs, while the left ventricle is responsible for receiving the oxygenated blood from the lungs and pumping it through the aorta and to the body [7]. The right and left sides of the heart exist as two separate pumps and perform very important, individual tasks. However, in a hypoplastic heart, these functions cannot be completed normally because of the underdevelopment of the left side of the heart, which is the crucial mechanical component in delivering sufficient amounts of oxygenated blood to the organs of the body [1].
HLHS is a collection of lesions and each case is unique in the extent to which the heart is malformed. Of all HLHS patients, 85% have some combination of atresia (congenital absence of normal opening or lumen) or stenosis (narrowing of any canal or orifice) of the aortic and mitral valves [9]. The remaining 15% have a common atrioventricular septal defect. On top of the malformations in valves of the heart, the left ventricle of the heart is grossly underdeveloped and in some cases is not present at all. These abnormalities result in inadequate heart function and thus reconstruction that is necessary to sustain normal metabolic function [1].
A hypoplastic heart has normal entry of the inferior vena cava and right superior vena cava into the right atrium; however, the right atrium is usually largely dilated. This enlargement, in addition to a larger tricuspid valve orifice, results in a hypertrophied (increased in bulk) right side of the heart (holding up to three times the normal blood volume). Along with the enlargement of right cardiac features, between 40% and 65% of patients have a posterior and leftwards displacement of the superior attachment of the septum premium relative to the septum secundum, resulting in the apex of the heart not being formed by the left ventricle but the right ventricle only. Because the left ventricle is not functional, pulmonary venous return must pass to the right atrium. This occurs either through an atrial septal defect, a stretched foramen ovale, or, in rare cases, by an anomalous pulmonary venous connection. Therefore, the right ventricle must maintain both pulmonary and systemic output [1].
The pulmonary orifice and main pulmonary artery are usually always enlarged and communicate with the descending aorta via the ductus arteriosus (connecting branch between the pulmonary arteries and aorta not seen in normal cardiac anatomy). Maintaining the presence of the ductus arteriosis is essential in attaining systemic perfusion. Otherwise blood would continuously circulate from the lungs to the heart and to the lungs again, not undergoing systemic circulation. The relative ratio of pulmonary to systemic blood flow depends on the delicate balance between pulmonary and systemic vascular resistances. If pulmonary resistance is too low, oxygenated blood will not undergo systemic circulation. The pathologic ailment of children with HLHS is an elevated arterial oxygen saturation resulting from high pulmonary blood flow, and thus marginal systemic perfusion resulting in metabolic acidosis [1].
2.1.3 CAUSE
The embryologic cause of HLHS is not fully known, however is thought to most likely result from either a reduction of left ventricular inflow or left ventricular outflow during development. Theoretically, a displaced septum primum may limit left ventricular inflow by obstructing the normal shunting of inferior vena cava blood through the foramen ovale to the left ventricle. This decrease in blood flow may result in a small left atrium, mitral valve, left ventricle, aortic valve, and ascending aorta. Other possible causes of HLHS include a congenitally small or absent foramen ovale and abnormalities of the mitral valve [1].
2.1.4 CLINICAL EPIDEMIOLOGY
While the incidence of HLHS is relatively low (1.4-3.8% of congenital heart disease), it has been reported to cause 23% of deaths in the newborn period. Approximately 1440 babies are born each year in the United States with HLHS. Because the disease is rare, about 20 of those cases are treated at Vanderbilt University Medical Center each year. There is an approximate 75% 3-year survival rate as children born with HLHS undergo surgery for this disease [1].
Children are diagnosed using fetal echocardiography, and in cases where HLHS is diagnosed sufficiently early, many parents choose to terminate the pregnancy. In the cases where HLHS presents itself within 24 hours of birth, it is usually because of severe obstruction to blood flow at the interatrial level. With this ductal impediment the patient develops metabolic acidosis and supportive treatment is necessary. Outside of the womb, electrocardiograms often reflect the underlying pathology showing no left ventricular signal [1].
2.2 CURRENT TREATMENTS
2.2.1 DRUG TREATMENTS
There are no drug therapies available to treat HLHS, however there are treatments that increase pulmonary resistance, thereby increasing systemic perfusion. Neuromuscular blocking agents accomplish this, and are administered preoperatively [1].
2.2.2 RECONSTRUCTIVE SURGERY
Goals of the reconstructive approach are to ensure systemic perfusion in the absence of a ductus arteriosus and to prepare the pulmonary vascular bed for an ultimate modified Fontan operation. There are three stages involved in the surgery, with each being very intensive and pervasive. The first stage of the three-step surgery is a surgical technique that reduces the inadequate supply of oxygenated blood to the body by placing in aortiopulmonary shunt. This allows blood to circulate from the right ventricle, through the pulmonary arteries, and consequently through the shunt and to aorta. After this first stage, the right ventricle is volume loaded and generates systemic pressure. This surgery has a mean survival rate of 73% for a 30-day hospital stay. Postoperatively, complications might occur as the aortic branch becomes obstructed (either in the distal or proximal arch). If this happens, immediate recognition is critical for the child’s well being. Another potential complication is the development of rapidly progressing cyanosis (blue or purple discoloration of the skin due to inadequate oxygenation) [1].
The second stage is called a hemi-Fontan or bi-directional Glenn shunt surgery, and is performed at about 6 months of age. In this surgery, the heart is exposed through a midline sternotomy. The superior vena cava and right pulmonary artery are dissected free, and a cardiopulmonary bypass is performed. Significant complications include transient superior vena cava syndrome, pericardial effusions, pleural effusions, phrenic nerve palsy, and death. The operative survival rate following hemi-Fontan is approximately 94% [1].
The third stage of the reconstructive surgery is the Fontan operation. This is performed approximately one year after the hemi-Fontan surgery. This procedure involves remodeling the placement of the superior and inferior vena cava. Approximately 45% of patients develop significant serous effusions, resulting in prolonged chest tube drainage post-operatively. The survival rate for the Fontan operation is 90%, with the majority of patients described as doing well from a cardiovascular and developmental standpoint [1].
2.2.3 HEART TRANSPLANT
The other method of treating HLHS is to perform a heart transplant. The main problem with transplantation is the availability of donors. If availability was higher, this method would be the dominant treatment option because operative survival for children who undergo transplants is excellent. However, between 10 and 40% of children with HLHS either undergo staged palliation or die while waiting for a heart. Thus, alternative solutions are needed [1].
2.3 DESIGN GOALS
The goal of our design is to eliminate the first two steps of reconstructive surgery while at the same time ensuring adequate systemic blood flow is achieved. Because the relative ratio of pulmonary to systemic blood flow depends on the balance between pulmonary and systemic vascular resistances, our device focuses on this relationship for treatment solutions. It is important to understand that when pulmonary resistance is too low oxygenated blood will not be circulated in sufficient amounts to the body. Thus, we have proposed a device that will increase the pulmonary resistance, thereby increasing the flow of blood through the ductus arteriosis and increasing oxygenated systemic blood flow [3].
3. METHODOLOGY
3.1 TIMELINE
We began research and brainstorming HLHS in December of 2002. The completion date for this device is April 22, 2003. In between these dates a consistent amount of work was completed each week. The first couple weeks were spent conducting research on HLHS and talking to Dr. Doyle about possible solutions. After intensive research, we acknowledged the complexity of our problem and realized the solution would not be easily attained. Moving from complex to simple approaches, we determined the design of our device by early February, 2003. Dr. Doyle was clear in defining the parameters of the device and the environment in which it will reside, and after weighing our alternative solutions we determined Nitinol as the most feasible material for this model.
Progress in our prototype creation was halted by our difficulty in finding a device in which we could test the effectiveness of our design. Because calculations were complicated and solving this problem has never before been attempted with this approach, the variable needed to solve for the exact dimensions of the device had to be obtained via in vitro testing. Finding and eventually creating a conical device was a slow process. After a week of shopping around Nashville, another week was taken to create a CAD drawing of the device to be sent to the NCIIA. From this point in time, another two weeks was spent waiting for the arrival of the prototype. Because of this delay in time, we were unable to complete the testing we had hoped to have originally finished to solidify the correct dimensions for the device. Ultimately, we concluded that in vitro testing would provide inconclusive results due to the unknown variables present in the testing design, such as availability of pulsating flow and inability to model vessel wall characteristics due to the static environment of the pipe.
3.2 DESIGN AND PROTOTYPE
3.2.1 BACKGROUND
Our device uses fluid dynamics of the heart and circulatory system to solve for inadequate systemic blood flow, and because we have not had extensive fluid dynamics courses, we had to seek the help of Dr. Mark Stremler (ME department) and Craig Russell (ME 2003). Their fluid dynamics equations to solve for the dimensions of the nozzle are included below:
One source (1) with three exits (2,3,4)
Q1 = 5*10-5 m/s (flow of blood from right ventricle to pulmonary arteries)
Q3 = Q2 +Q4 (same amount of blood goes into lungs as organs)
d2 = 0.0035 m
Find: size of conical nozzle
Solution:
Conservation of mass:
Q1 = 2v2A2 + v3A3
5*10-5 = 4 v2A2
For single nozzle:
v2 = Q2/(Õd22/4)
v2 = 1.3 m/s
conservation of energy: