On Tuesday (May 18th) Nancy is scheduled to have an examination meeting with an assistant of the doctor who will soon outfit her with an implantable cardioverter defibrillator (ICD). There are many pages on the web that can be found using this 3-word phrase. However, the basic concept is that of using something to provide an electric impulse to convert an abnormal heartbeat into a normal heartbeat. Just a few years ago there was interest in (chemical) medications to accomplish cardioversion (the conversion of one cardiac rhythm to another) but rapid development of implantable devices (following the introduction of the simple pacemaker) has driven the modern usage to be synonymous with defibrillator. We’ll get to that in a bit.
A Canadian named John Hopps was trained as an electrical engineer (EE) and conducted research on treating hypothermia (cold core body temperature). While experimenting with radio frequency heating to restore body temperature, Hopps made an unexpected discovery: if a heart stopped beating, it could be started again by using an electric impulse. By 1950 he had developed a rather large device that could be used (externally) as a pacemaker. Shortly after that another EE named Wilson Greatbatch had his own eureka moment that inspired his invention of the implantable cardiac pacemaker, and following that he developed the corrosion-free lithium battery to power it. Wilson Greatbatch is thus considered the inventor of the pacemaker.
The 60 years following these early inventions has seen rapid progress in understanding the electrical nature of the heart, electrical-electronics concepts, and miniaturization capabilities.
The heart is a 4-chambered muscle with blood from the body seeping into one chamber from which it is then forced out when the muscle contracts in response to a body-generated electrical pulse – the beginning of the heartbeat. That impulse is developed and sent out from the sinoatrial node, often called the SA node. This is located on the inside surface of the upper-right part of the heart in the Right Atrium – the chamber into which oxygen-depleted blood from the body seeps. When this chamber contracts blood is sent to the chamber below it – the right ventricle – by way of the tricuspid valve. The blood in the right ventricle will go to the lungs for a fresh supply of oxygen.
Re-oxygenated in the lungs the flow from there is collected in the left atrium, also an upper chamber. That blood will next pass into the lower chamber on the left – the left ventricle – which is the largest chamber of the heart and its contraction forces blood out into the body. The more the wall muscle is stretched, the more forceful the contraction and the better the body’s cells receive oxygenated blood. The mitral valve opens to allow the flow from the left atrium into the left ventricle. It closes for the contraction so that the blood goes out into the body and not back up into the left atrium.
There is a lot to go wrong as the heart beats, pressures rise and fall, valves open and close, and blood flows. The electrical impulse that starts in the SA node in the upper right has to move in perfect rhythm to the different parts such that each job is done in collaboration with the others. One of Nancy’s major problems – now fixed – was the poorly performing mitral valve. Because some of the blood was forced back into the chamber above it, the blood from the lungs seeping into the left atrium was encountering pressure that should not be there. That blood should have been going through the aortic valve, into the aorta – the major artery supplying fresh blood to the entire body. The imbalances of pressures and the leakage caused the heart to enlarge.
Also, the left atrium contraction fills the arteries that supply the heart muscle with oxygen. The two main arteries (lying on the outside surface) of Nancy’s heart were narrowed and this was the site of the clot that sent her to the ER on Friday following Thanksgiving. The lack of oxygen-rich blood to this part of the muscle caused damage/death to some of the cells of the heart wall. Thus, it doesn’t stretch and contract as it should. Furthermore, (the following seems reasonable to me but I can’t find a web article to confirm it) the stretching and dying of the heart wall should alter the paths and timing of the electrical signals flowing down through the heart. It seems to me that the heart is working around this damage but is more likely to loose its natural rhythm (experience arrhythmia). When the left ventricle is experience this loss of natural rhythm it is called ventricular fibrillation (v-fib) and instead of stretching and contracting normally the muscle quivers rapidly and irregularly.
When this happens, the heart pumps little or no blood to the body. V-fib is fatal if not treated within a few minutes. Most cases of sudden cardiac arrest (SCA) are caused by ventricular fibrillation. What actually sets the heart into v-fib is another matter but studies show that it is more likely to happen when the efficiency of the heart as measured by the ejection fraction is below 35%. Scroll back to the page for SUNDAY – April 25th where, in the bottom part, this is explained further.
If any part of the heart is experiencing fibrillation (and it is serious) than the solution is to convert it into a normal rhythm, and thus is born the term defibrillation. The thing that does this is a defibrillator based on the idea of the conversion of a bad rhythm into a good rhythm. Modern science and medical technique now can miniaturize the necessary components, doctors can implant the unit under a person’s skin with leads to the heart and should the fibrillation occur the patient is saved by the implanted cardioverter defibrillator (ICD).
Simple really. We are off to the heart clinic on Tuesday to set the plan in motion.