So here I was, gasping for air, after swimming three laps (150 feet) in the Oakhurst pool. Since I normally do 30 laps (1500 feet), with hardly an increase in air intake volume, there was something terribly wrong. I knew what it was and, because there are lots of other people in the same boat, the purpose of this essay is to get them to do something about it.
As we all know, exercise requires muscle contraction, which requires energy via oxygen burning up fat. To meet the demand, the body increases air-breathing rate and it increases heart rate [beats per minute (BPM)]. If you can’t increase the oxygen supply, you can be in deep trouble. On a short-time basis, you can become dizzy, or faint (syncope), or end up gasping for air, and have an inability to do sustained work. On a long-time basis, if body organs are chronically deprived of oxygen, they deteriorate; as in the proverbial “one-hoss shay,” collapse will follow.
By way of background: a normal heart is depicted in Fig. 1. From a “block diagram” viewpoint, the heart is simplicity personified: Oxygen-poor-carbon-dioxide-rich blood returns, through the venae cavae, into the right atrium. From here it goes through the tricuspid valve into the right ventricle. The latter pumps the blood, through the pulmonary valve, into the lungs. Oxygen-rich-carbon-dioxide-poor blood from the lungs returns into the left atrium. From here it goes through the mitral valve into the left ventricle. The latter pumps the blood, through the aortic valve, into the aorta.
Fig. 1- Cross-sectional view of the human heart that shows the direction of normal blood flow.
Figure 1 does not indicate the timing cycles, which are also very simple. During the diastole period, the heart muscle relaxes and the atria fill up. At the start of the systole period, both atria contract together, forcing blood into the ventricles. About 0.15 second later, the ventricles contract together, forcing blood into the lungs and aorta. The valves, of course, prevent the backward flow of blood.
Like any muscle in the body, contraction depends upon and follows stimulation by an electrical “action potential.” This is illustrated in Fig. 2. The sino-atrial node initiates the electrical heartbeat impulse. This signal (delayed) is picked up by the atrio-ventricular node, which initiates stimulation of the ventricles.
Fig. 2- Cross-section showing the heart’s natural pacemakers, the sino-atrial and atrio-ventricular nodes.
In my case, the heart muscle was great—but it only did 30 BPM! A normal heart rate is 60 BPM. Gasping for air didn’t help in the least—with insufficient blood available to absorb oxygen from the lungs and carry it to the muscles, there was nothing to do but slow down to three laps followed by rest.
But let me back-track a bit. My normal heart rate for years was 40 BPM (the athletic type). Then Dr. W noticed, from an electrocardiogram (ECG), that the signal from the atrium to ventricle was excessively delayed. The diagnosis was “Heart block of the first degree.” What is that all about? A fairly common age-related deficit (ARD) is the failure of the atrium-ventricle signal. What to do about it? Nothing—if it is of the first degree. But as Dr. W said, casually, “If it becomes a third-degree (or complete) block, and your heart rate drops down to 30 BPM, you will need a pacemaker.” One of the important ingredients today, in increasing the life span of ARD victims, is the invention of the pacemaker.
It is a highly unlikely device. Imagine walking around with wires threaded into your heart and, yet more frightening, they deliver a “healthy” shock to the heart muscle! Biomedical engineers were knowledgeable, of course, about such matters, but major problems had to be solved before one could extend a patient’s life with a pacemaker. In 1958, Wilson Greatbatch finally developed the first successful implanted device. Since then, many biomedical engineers have continuously labored, (and continue to labor) to improve the pacemaker by applying advances in materials, microelectronics, batteries, and lead technology. Today, over 250,000 patients worldwide receive a pacemaker each year;
As luck would have it, one fine day, I couldn’t eat my porridge. Not enough blood circulating to digest a lousy bowl of oatmeal! This was serious. I called Dr. W and came in prepared to do battle. “We are leaving for Canada in three days.” Dr. W, with a look of horror as he perused my ECG, came back with “You are leaving for Memorial Hospital immediately.” My wife, who hasn’t driven for 40 years, took over the wheel. The transformation from being human to being a patient was complete and devastating. At the Hospital, I became a helpless invalid whose heart could stop at any moment.
The next day, under anesthesia, Dr. C installed a two-lead (two-chamber) pacemaker. The details are pictured in Fig. 3. The tip of one lead is positioned in the right atrium, and the other lead in the right ventricle. Notice that the ventricular lead passes through the tricuspid valve, which is supposed to close properly around the lead. The heart, a dumb mechanical contraption that does not have a mind of its own, was being zapped at a resting rate of 50 BPM. (With a normal rate of 40 BPM, Dr. C agreed that the paced rate should be 50 BPM.) Instant and complete recovery! Out of sight of the nurses, I ran up and down the hall.
Fig. 3- Cross-sectional view of the human heart, with a pacemaker on the left side of the patient, showing its dual-chamber leads. One lead is attached to the wall of the right atrium; the other to the wall of the right ventricle.
Usually, in a single-chamber pacemaker operation, the single lead goes to the right ventricle.
The badge of honor—a two-inch disk—is clearly outlined underneath the skin below the left collarbone. It is powered by a small battery that has a life, typically, of six years. The battery is of a type (lithium-iodine) whose voltage slowly decreases as it runs out of power; when the voltage drops to a predetermined low value, the disk pocket is opened (minor surgery), the leads are unplugged, and the unit is replaced.
Back at the Oakhurst pool, the inmates, many of whom have pacemakers, were again upset because I made waves for 20 minutes while they were doing their anti-arthritic exercises.
One of the most fantastic parts of the system is how the pacemaker is monitored for battery voltage and general behavior. Every two months the patient gets a “telephone check”: At a prearranged time, the patient attaches wrist-band electrodes from a kit that has been supplied by the Heart Center. The wrist signal is processed and fed to a small loudspeaker, which “talks” to the mouthpiece of your telephone. (It is fun to place your ear close to the loudspeaker and listen in to the conversation: a high-pitched whine modulated by your heartbeat.) After the normal signal is recorded, the technician asks you to place a magnet (supplied as part of the kit) over the pacemaker. The magnet closes an internal switch that causes the pacing speed to increase to 100 BPM. From the new and previous data, the technician can extract information about battery voltage, and so forth.
The telephone checks are replaced, periodically, by personal visits to the Heart Center, where external leads are attached to the patient, as in a conventional ECG recording session.
The pacemaker contains microcircuitry that enables many characteristics to be adjusted by the heart surgeon and technicians. They can communicate with the implant, via wireless, through a loop held over the pacemaker disk. They can adjust the resting heart rate, time width of the trigger pulses (typically 0.4 millisecond), trigger pulse amplitude (typically 3.5 volts), delay between atrial and ventricular pulses, and much more. Based on the output of a tiny accelerometer, the pacemaker increases your heart rate if you become active. Perhaps most important is that the atrial and ventricular leads pick up the heart’s own electrical signals, and the pacemaker is programmed to compensate, accordingly, for indications of abnormality.
The pacemaker is, indeed, a very intelligent robot that annually extends thousands of lives at relatively low cost.
But Don’t Stretch That Pacemaker Arm! Since this is not supposed to be a mystery story, I will immediately reveal that my pacemaker ventricular lead became defective. Very rare, I was assured by my cardiologist, Dr. C. But, somehow, many of my friends remembered similar cases, and that this fantastic system is vulnerable to all kinds of “accidental” and deadly defects. Typically, to duplicate a normal heart beat, my two pacemaker leads deliver a 3.5-volt shock, with the ventricular pulse lagging 0.15 second behind the atrial pulse.
Three years before, my heart paced itself at 30 beats/minute on its own. (Since this is abnormally low, it was the reason for the pacemaker.) Now, without the pacemaker signal, the heart didn’t do a damn thing. Just sat there stupidly waiting to be kicked. It is a great way to die: There is an overwhelming strange feeling that something is terribly wrong. Muscles relax. Fear sets in for 10 seconds. After that, my cardiologist assured me, you lose consciousness.
Here is the chronological sequence:
Monday, 1 April, 2002: (This narrative is not an April Fool’s joke.) While doing nothing in particular, I got hit with a short near-fainting spell. Although this wasn’t supposed to happen, but it only lasted a few seconds, I ignored it.
2 April: Attacks continued. In the afternoon I drove (with Ruth by my side) to Dr. W’s office. Because the defect didn’t show up, he couldn’t find anything wrong. But he did point out that the wheel has been invented, and perhaps I should use a rolling suitcase instead of the arm-supported he-man variety.
3 to 5 April: I kept driving the car, convinced that the fainting spells were caused by abnormally low systolic pressure. I was confident that each attack would only last a few seconds. I didn’t have the heart to deprive my passengers of restaurants, plays, concerts, and so forth. And everybody was lucky; I got away with it!
On Friday afternoon, 5 April, I noticed that raising my left arm, which pulls on the leads, usually brought on an attack. So that’s what caused it, a defective lead! The timing was perfect: I wouldn’t dream of calling the cardiologist late Friday afternoon (which is when these discoveries are always made). It would have to wait until Monday morning. In the meantime, Ruth tied my left arm close to my body to keep me from inadvertently raising it. I continued to drive, of course.
Until Sunday, 7 April. As every electrical engineer knows, bad connections get worse. I had a long-lasting frightening attack in the morning. Ruth was too upset to drive, so I asked a friend, MH, to drive us to Emergency.
They wheeled me into the room (patients are never allowed to walk into Emergency). I proudly told the staff that I had diagnosed the problem. They hooked me up to an electrocardiogram (ECG) monitor. “Raise your left arm over your head. Yup, you have a defective lead, alright.” I was soon surrounded by clinicians along with the cardiologist on duty, Dr. K. The pacemaker manufacturer’s representative also appeared out of nowhere; in retrospect, perhaps this was to “calm me down” to keep me from suing them for negligence.
Ruth and MH went home. After a while, Dr. K sent me to the Heart Patient section, Intensive Care, where they could keep an electronic eye on me.
I was hooked up to a Shocking Machine, commonly known as a defibrillator. At one point, I watched myself die as my heart stopped for nine seconds and the ECG trace became a horizontal line. Alarms went off and everybody came running, but the heart recovered. Dr. K set the controls on the Shocking Machine so that it automatically gave me a shock (yes, it was painful) when the pacemaker failed. The only way to avoid the shocks was to remain absolutely still. I became a sort of celebrity: The usual patient in Heart Intensive Care is half, or about to become fully, dead. The nurses, even from other departments, came in to stare at this guy who sat up in bed shaking every once in a while, told them how great they were, and was reading the IEEE Spectrum.
8 April: At 1 PM, just when I got used to the painful shocks, Dr. C snaked a temporary lead from my groin to the heart, attached to a temporary pacemaker. The temporary shocked the heart without pain because the signal was inside the heart. At 4 PM I received a new pacemaker and new ventricular lead. The faulty lead was disconnected but left in; it was too dangerous to remove it. So what went wrong? I am not volunteering to get that question answered. I think it was not a complete break, which would have been deadly, but an electrical leak that sometimes reduced the pulse level below threshold. The manufacturer’s representative assured me that some patients eventually end up with five leads side-by-side (one active, the others unused). Not to worry; plenty of room in the vein.
9 April: I was discharged, completely cured! I was asked to take an antibiotic (8 monster pills at $9 per pill). A friend drove me home.
What has happened since the April episode? How could I sue Drs. W and C for negligence?—After all, they saved my life three years ago. Instead, I filed a “MedWatch” complaint with the Food and Drug Administration:
“The entire industry is at fault. The cardiologist, and the instruction booklet that the patient gets, should be required to caution the patient to minimize stress on the leads; try to avoid stretching the arm (on the pacemaker side) above the head. It is negligent to omit mention that the leads can become defective. The 2002 booklet has a figure that shows a patient swimming and stretching the arm; this should be avoided.”
[I changed my life style. Now I swim on my back, using the right arm to propel the body, and fellow-swimmers are happy because I no longer make waves. With the new swim stroke I can watch the birds and airplanes flying overhead, none of that chlorinated water gets into my eyes, and my dentures stopped falling out. Since I can’t see where I am going, I keep bumping into other pool occupants (mostly women, as luck would have it, since the men folks and their pacemakers are gone.)]
Yes, Food and Drug sent a form-letter acknowledgment that my report has been received. There the matter rests, perhaps RIP.
(Published in a shorter version in IEEE Engineering in Medicine and Biology Magazine, Sept/Oct 2002)