Stephen B. Knisley
Professor of Biomedical Engineering
Tamara C. Baynham
Biomedical Engineering Ph.D. student
University of Alabama at Birmingham
If you’ve ever listened to a healthy human heart, you’ve heard its soft, rhythmic beating. However, for about 4.3 million Americans who experience arrhythmias, their heartbeats are anything but rhythmic. They may even be life threatening. Arrhythmias factor into half of all sudden cardiac deaths in the United States each year.
There are treatments for arrhythmia, including medications and electronic devices called automatic implantable cardioverter/defibrillators (AICD). But researchers at the Cardiac Rhythm Management Laboratory at the University of Alabama at Birmingham are trying to improve AICDs by evaluating new options for the most effective shapes and positions of electrodes on heart fibers. They are also learning more about the structure and electrical behavior of the heart.
SIMULATION AND ANALYSIS
Current AICDs electrodes, called point electrodes, are essentially small cylinders or the rounded tips of wire leads. When they emit electric current, it spreads radially from the source much like ripples spread across the surface of a pond when a pebble is dropped into it. However, heart fibers resist the current, causing an uneven spread of current and a nonuniform distribution of transmembrane voltages. Researchers wanted to develop techniques that would create more uniform changes in transmembrane voltages and more efficiently halt ventricular fibrillation, the most deadly form of arrhythmia.
One possible way to reduce resistance and homogenize voltages involves orienting the electrode with respect to the direction of heart fibers But point electrodes cannot be so oriented. Researchers hypothesized that, by using a line electrode instead of just a point, it could be positioned either parallel or perpendicular to heart fibers to better transfer current and create more uniform distributions of transmembrane voltages. (A line electrode can be a series of point electrodes arranged in a line or an entire segment of exposed wire applied directly to the heart.)
Before researchers could test this hypothesis, they needed to determine the current density or distribution emitted by a line electrode. Up to this point, classical electrodynamic theory had only been applied to conventional shapes, such as disk-shaped electrodes with radial symmetry. From classical theory, researchers knew that more current is emitted from the edge of a disk electrode than from the center. It was possible, then, that a line electrode might emit more current from its ends than from the middle segment. Researchers used simulation and electrostatic analysis software from Algor Inc., Pittsburgh, Pa., to get an idea of just how much current would be emitted from each point on a line electrode.
Using Algor’s Superdraw III, a precision finite-element model-building tool, researchers modeled a 100 X 100-cm sheet, which represented a conductive area of the heart. They applied a resistivity value based on a thickness of 1 cm to simulate a uniform resistance over heart fibers. A 3.6 X 3.6-cm central region contained a 1-cm long electrode in the center. Voltage boundary elements were applied to points on the sheet that were in contact with the electrode.
Smaller two-dimensional planar elements surrounded the electrode for more detailed results in this area of concern while larger elements were used for outlying areas. Researchers specified that 100 V be applied at the electrode and that the voltage would be zero at the perimeter of the sheet. They found that values chosen for the voltage and resistivity affected the total current, but did not affect current distribution along the electrode. The finite element model showed that current at the ends of the electrodes was 151% greater than current near the center. The researchers also used FEA to determine that the length of the line electrode does not affect current distribution.
PROVING IT IN THE LAB
To confirm the FEA results and further test the positioning of the electrode with respect to heart fibers, researchers applied line electrodes in varying positions and orientations on 13 rabbit hearts. Rabbit hearts were used because their fibrous structure is similar to human hearts. Furthermore, rabbit hearts are about the size of a small peach and easier to study because they need little artificial blood to keep them “alive.”
Researchers first applied line electrodes parallel to heart fibers to see if the transmembrane voltage moving through fibers would be uniform, as was hypothesized. Producing an efficient change of voltage from very irregular to uniform is vital to restoring regular heart rhythms.
The magnitude of changes in transmembrane voltage on either side of the electrode remained constant or increased in the central region for the first few millimeters away from the electrode and then began to decrease. The most significant magnitude changes in transmembrane voltage occurred at the electrode ends. This correlates with the results of the electrostatic analysis, which showed a high concentration of current in this area.
Next, researchers oriented the line electrode perpendicular to heart fibers. The results indicated that changes in transmembrane voltage were less uniform across the fibers. Notably, the change in transmembrane voltage could be positive or negative. The changes in transmembrane voltage had the same sign (i.e., were more uniform) when the line electrodes were parallel to heart fibers.
FROM THE LAB TO THE CLINICS
Line electrodes give designers better control over transmembrane voltages, making them more uniform and homogenous, closer to that of a normally functioning heart. This knowledge could be applied to future AICDs that would regionally block areas of the heart from getting out of sync and prone to fibrillation.
Furthermore, line electrodes may play an important role in developing new, less invasive therapies for arrhythmias, including the insertion of several line electrodes into the heart through cardiac veins for treatment. Distributing electrical stimuli from several electrodes may be a more efficient way to apply current to the heart. It would also be less traumatic than alternative methods that require surgical procedures to open the chest.
In conclusion, researchers determined the distribution of transmembrane voltage changes from a line electrode. In the future, electrodes of other shapes can be studied using FEA to determine potential advantages of new configurations.
There are several kinds of arrhythmia and treatment differs for each. Excessive slowing of the heart often requires implanting an electronic pacemaker to speed and strengthen the heartbeat. Arrhythmias that speed up the heart rate are further classified as either atrial or ventricular fibrillation, depending on which chambers are affected. Atrial fibrillation causes about 15% of strokes per year by causing blood clots that have developed in the atria to move to an artery in the brain, according to the American Heart Association. This type of fibrillation is often treated with anticlotting medication.
Ventricular fibrillation, the most serious type, contributes to many of the 250,000 sudden cardiac deaths in the U.S. each year. Ventricular fibrillation must be corrected immediately, and the only way to do that currently is with electric shock. Cardiac rhythm, once restored, is maintained with medication or an electronic device called an automatic implantable cardioverter/defibrillator (AICD).
In recent years, more physicians are turning to AICDs because studies show them to be as effective or better than medications. What’s more, not all patients who survive fibrillation can be effectively treated with drugs. Because fibrillation occurs across all age groups, AICDs provide an alternative to lifelong medication and improve the overall quality of life.
AICDs consist of batteries and a pulse generator insulated in a flat case, which is inserted under the skin. Insulated metal wires from the case run through veins to position electrodes directly within the heart. Sensor electrodes detect when the heart is out of rhythm and signal the pulse generator to send an electric current through an exposed electrode. This quickly halts fibrillation.
A normal healthy heart is a muscle about the size of an orange that pumps thousands of gallons of blood each day through the arteries, veins, and capillaries of the circulatory system. Blood supplies all parts of the body with oxygen and nutrients while also removing waste from cells.
The four chambers of the heart, the upper left and right atria and the lower left and right ventricles, must work in precise order to pump efficiently. A specialized group of cells located in the right atrium, the sinus node, sends electric impulses at regular intervals through heart fibers of the atria and ventricles. As the electric impulse moves through the fibrous membrane of the heart, muscle fibers in the heart contract, pumping blood, and then expand as the signal passes, letting blood refill the chambers. Throughout this contraction/ expansion cycle, the mount of current or voltage across the heart fibers, called transmembrane voltage, continually changes.
For a normal heart, the distribution of the transmembrane voltage is approximately uniform throughout the heart. If values differ greatly, arrhythmia can occur as the electric impulses of the heart become disorganized. Heart disease or blocked arteries often cause this disorganization. For example, if an artery serving the heart is blocked, blood flow to that part of the heart stops and that part of the heart might respond only weakly or lose all function. The heart then loses its synchrony because all its parts are no longer functioning properly and arrhythmia arises.
Arrhythmias can make the heart beat slower or faster than the normal rate of 60 to 100 beats per minute. This can lead to a potentially fatal condition called ventricular fibrillation where the heart quivers instead of pumping blood. If left untreated, the patient dies within minutes.