is working entirely on its own, the foramen ovale closes during the first few days of life. With that connection blocked, the right side of the heart now pumps blood into the pulmonary circulation system of the lungs,* and the left side pumps blood round the rest of the newborn baby’s body.
In the theatre, this is the stage when the first signs of conflict usually appear. The same is true of the heart. If something has gone seriously wrong with the development process of the heart, this is when it will become known, if it hasn’t already. Although prenatal diagnostic techniques are now very advanced in the developed world, they are still not perfect, unfortunately. When doctors listen to an abnormal infant heart, they will often be able to diagnose a heart defect based on the sounds they hear.
The most common of these is what doctors call a ventricular septal defect, when the wall dividing the heart’s two ventricles has a hole in it.† In the most serious cases, a young life must begin with major heart surgery. It depends on the size of the opening. Minor defects can heal up by themselves without any medical intervention, and as long as the newborn child appears to be vigorous and thriving, there is no immediate danger to the baby’s life. The decisive factor is whether the infant’s organs are receiving enough oxygen. If this is the case, then doctors, parents, and, most importantly, junior can breathe easy.
Act Three: the strong heart
The heart of a healthy 20-year-old human contracts somewhere between 60 and 80 times a minute. If it is well trained, it can beat quite significantly more slowly when its owner is at rest. And this bundle of muscle is practically bursting with energy. The best way to gain an idea of its internal structure is to cut it open and take a look. For me, as a student of medical anatomy, this was an extremely exciting experience. But it might not be everyone’s idea of fun.
Let’s take a look at it from the point of view of a red blood cell, also known to scientists as an erythrocyte. It, and its many fellow red blood cells, gets its name from the red pigment haemoglobin, which it contains. Its main job is to transport oxygen from our lungs to the rest of our body, and, on return, to transport carbon dioxide back to our lungs.
Imagine you are an RBC (the slang term among medical types for red blood cell). You are transporting carbon dioxide — bonded to your haemoglobin — from one of the organs of the body, let’s say the brain, through a blood vessel back towards the heart. So you must be in a vein, since that’s the term for all the vessels that transport blood to the heart, while those that carry blood from the heart to the rest of the body are called arteries. After a few twists and turns, you eventually end up in the superior vena cava, a vessel that empties directly into the heart. And it is into the heart’s right atrium that you are now swept, along with your cargo of carbon dioxide. From there, you pass into the right ventricle of the heart. Hurry now, don’t dawdle, we have a mission to complete!
To get from the heart’s right atrium to the right ventricle, you pass through an atrioventricular valve known to medics as the tricuspid valve (the Latin word cuspis means ‘point’ or ‘tip’). Once you have left the right atrium via that valve, there is no going back — if you are in a healthy heart. All the heart’s valves are unidirectional: they only let blood flow one way. This is a trusty means of making sure blood does not flow in the wrong direction, from the right ventricle back into the atrium. Thus, in a healthy heart, blood always only flows in one direction, and does not, for example, slosh back and forth between the ventricle and the atrium.
Continuing your journey, you leave the right ventricle via another valve — the pulmonary valve — heading towards the lungs. Having passed through that valve, you now find yourself in the pulmonary artery, the artery of the lung. This shows, by the way, that the much-quoted rule ‘arteries transport oxygenated blood and veins transport deoxygenated blood’ is in fact nonsense. After all, you’re still carrying your cargo of carbon dioxide, making you ‘deoxygenated’, although you are currently floating through an artery, not a vein. Once more for clarity, the more accurate rule is: arteries carry blood away from the heart, veins towards it (although there are still some small exceptions to this rule, e.g. in connection with the liver*).
On arrival in the lungs, you complete the first part of your mission as an RBC by unloading your carbon dioxide and taking on a fresh cargo, this time of oxygen. With that freight on board, you now set out on a return journey through the pulmonary vein (!) back towards the heart. There, you and your many fellow erythrocytes flow into the left atrium and on, through a third valve, into the left ventricle, the last ventricle on your voyage. The valve between the left ventricle and the left atrium is known as the bicuspid† or mitral valve, so called because its shape reminded anatomists of the kind of bishop’s hat known as a mitre.
The left ventricle is the bodybuilder among the chambers of the heart. It has by far the thickest muscle wall. This isn’t surprising, since it needs to build up a great deal of pressure to keep our blood constantly flowing and to pump it to even the furthest reaches of our body. Now, on we travel, through a final valve, the aortic valve, and into the aorta, the body’s main artery. This vessel describes a graceful curve around the heart, from which vessels branch off towards the head and the arms. It then continues into the abdomen, where it splits into ever-smaller branches to provide fresh blood to all our organs and tissues, right down to the tips of our toes.
We are now approaching the climax of our drama of the heart. Everything is working fine, the heart and vascular system seem to be indestructible. But things are about to take a tragic turn.
Act Four: the ailing heart
After just 25 years, the first ‘deposits’ begin to appear on the walls of the coronary arteries (arteries that supply the heart muscles themselves with blood). At this stage, it’s not a big problem, but it lays the foundation for a very serious condition: arteriosclerosis, sometimes called ‘hardening of the arteries’. It is the number-one cause of the world’s most-common killers: heart attacks and strokes. Deposits of fatty plaques on the walls of the blood vessels will continue to build up, getting thicker and thicker and restricting the flow of blood until, in a worst-case scenario, a vessel eventually becomes completely blocked (like a water pipe with limescale).
When this happens to the coronary arteries, small or even larger sections of the heart muscle are left with an insufficient supply of nutrients and oxygen, and they begin to change. This is the infamous heart attack. Undersupplied areas of muscle transform into a kind of scar tissue that no longer contributes to the beating action of the heart. And, as we all know, a team is only as strong as its weakest member. The result is that the heart loses both strength and stamina.
At this point in a play, drama theorists speak of a ‘delaying factor’ in the plot, when the pace of the story slows down as the final denouement approaches. In the case of heart-attack patients, the role of delaying factor is played by medicine. To delay, or, even better, avert the oncoming catastrophe, doctors can prescribe medication, insert catheters (thin plastic tubes) into the coronary arteries, and try to alter the patient’s life circumstances to take some pressure off the heart and thus minimise the risk of another heart attack.
Act Five: the (c)old heart
Chest pain. Irregular heartbeat. A listen to the chest with a stethoscope shows it is no longer beating with its regular ba-boom, ba-boom, ba-boom rhythm. Now, it sounds more like ba … boom, ba-ba-boom, boom, ba-boom. Difficulty breathing and weakness set in. After beating without a break for almost a century, the heart is now significantly weaker. It’s been through a lot. For some, it may be experiencing its second or third attack. It pumps ever less powerfully and, in a final act of valour, it gathers all its resources and tries to work faster. But in the end, all is in vain. The heart is no longer able to work properly; it twitches uncontrollably for a brief while and eventually becomes still. And then that’s it: curtains.
This is the inescapable end to the drama. Predictable, but nonetheless tragic. Although all of our hearts will eventually stop, the time before this happens need not be dramatic. On the contrary, a hale and hearty life is more reminiscent