How the heart works

In this video, we are going to look at how the heart works. We know that the heart sits in the center of the adult chest, with about a third of it off to the left-hand side. And structurally it’s made up of four chambers which are filled with blood. It’s separated into a left side and a right side; the right side providing the circulation to the pulmonary circulation in the lungs, and the left side supplying blood out to the systemic circulation and the organs around the body. The heart is unique in that it’s made up of hundreds of thousands of tiny myocytes, which generate electricity. These are structured so that they cause the chambers of the heart to contract, forcing the blood through the four chambers of the heart in one direction only. This is controlled by valves which open and close, according to the pressure in the chambers. The electrical conduction system of the heart starts with the sinoatrial node, or the SA node. And this is generally considered to be the pacemaker of the heart, which is under control of the nervous system. When the electrical impulse leaves the SA node, it travels across the atria and it arrives at the AV junction, or the AV node. This has got the function of slowing down the electrical impulse to allow blood to pass from the atria, through the atrioventricular valves, and into the ventricles. Now, this takes time.

So the AV node acts as a gatekeeper. It keeps all of the electrical impulse, and then passes that signal down through the bundle of His into the left and right bundle branches, out to the Purkinje fibers. And this in turn then initiates a wave of depolarization across the ventricles, causing the muscle to contract, and ejecting blood out into the pulmonary and to the systemic circulation. What’s also important to remember is that if we take the heart out of the body so that it’s just an individual organ, it will continue to beat probably around about 120 beats per minute until it runs out of oxygen and nutrients, and it will eventually die. But what’s important there is the fact that the heart doesn’t beat at 120 beats a minute when it’s in our bodies. It’s under the control of the vagus nerve, which slows down the rate of conduction to a rate that our body needs to maintain blood pressure and organ perfusion. Now, if something goes wrong systemically, I.e. The patient’s shocked, they have a fever, they become hypothermic, then the nervous control over the heart is affected. And when we determine in our treatment regimes for tachycardias and bradycardias, we must first identify whether the tachycardia or bradycardia is caused by an extrinsic factor or something intrinsic. And by that I mean, are we looking at something that’s causing the vagus nerve to be overstimulated?

Are we looking at shock, where we have got fluid failure, or pump failure, or container failure even, and the heart’s having to work faster and faster and faster to keep the blood pressure high so that it can perfuse the brain and the organs? We can establish whether the cause of the tachycardia and bradycardia are intrinsic or extrinsic by recording an ECG rhythm. If we establish that the tachycardia is caused by an intrinsic factor, then our whole treatment regime is different. Given that every cell in the heart is capable of generating an electrical impulse, when everything’s under tight control of the nervous system and the heart’s well-perfused with oxygen and nutrients and everything’s working nicely, we would expect the atria to contract, the ventricles to contract, and that system sequence to continue. When there is a problem in the heart, when parts of the heart become ischemic due to coronary artery disease, then we can expect to see a malfunction in the electrical conduction system. An area that gives us problems with the rhythm of the heart, and one that often causes tachycardias, is when the AV node becomes hypoxic and we start to develop re-entry tachycardias. This is essentially a shortcut in the electrical conduction pathways.

The electrical impulse circulates around the ischemic area and speeds up, becomes faster and faster and faster. And we often see rates of in excess of 200 beats per minute in what we term as supraventricular tachycardias. When the heart’s beating normally, each chamber contains approximately 70 milliliters of blood. It takes time for that blood to travel between the chambers. So at 60 beats per minute, there’s enough time for that blood to travel from the atria to the ventricles, and then the ventricles to contract for that blood to be shifted out of the heart. But as the heart rate increases, perhaps to upto 120 or 180 or 200 beats per minute even, as we see in the tachycardias, it’s easy to see how there’s just not enough time there for ventricular filling, and therefore the amount of blood ejected from the ventricles during systole is reduced.

Now, this has a consequence of reducing cerebral perfusion, blood pressure, and other organs which need… For example, your kidneys need approximately 60 millimeters of mercury, systolic pressure, to perfuse. As the heart rate increases to a point where the ventricles have no longer got time to fill, we start to see symptoms of shock developing in the patient. This could be pale, sweaty, clammy, breathless, altered levels of consciousness, and the patient may become incoherent. Our management of the supraventricular tachycardias requires us to simulate an increased handbrake pressure on the heart, which is what the function of the vagus nerve is. It acts as a handbrake to slow the intrinsic rate from 120 beats per minute down to approximately 60 or 70, depending on the patient.

Now, we can achieve this in our initial management of a supraventricular tachycardia by applying pressure to the carotid sinus. By doing so, we almost trick the carotid sinus into thinking that the blood pressure is higher, and it will innervate the vagus nerve and stimulate the vagus nerve, and inhibit the impulses from the SA and the AV node, thus slowing down the heart. If this fails, there are drugs we can use in the management. And our first drug to use in a narrow complex supraventricular tachycardia would be Adenosine. Adenosine acts by blocking the impulses momentarily through the AV junction. Our initial dose is 6 mg, given rapidly IV, which can be repeated in 12 mg doses, and again at 12 mg doses in three to five-minute intervals. If, when we’re looking at the ECG of our patient who was in tachycardia, and the rhythm is a broad, complex rhythm, then our management regime is different. And we initially start off by administering Amiodarone intravenously of a 10-20 minute interval in order to slow down the electrical impulses through the conduction system. Amiodarone has the effect of slowing down the repolarization rate of the cardiac cells, thus allowing the SA node to take over as the pacemaker of the heart.

If Amiodarone doesn’t work and the patient becomes less responsive, or becomes symptomatic with an altered level of consciousness, then we will need to deliver a series of DC shocks to try and stun the heart so that the SA node can take over as the pacemaker. We do this by attaching the defibrillator paddles to the positions that we’re familiar with, and then we deliver three shocks at 125 joules, 125 joules, and 150 joules. Now each area, each trust, each organization will have its own policies on the joulage to shock the patient at. In the pre-hospital environment we use 125, 125, and 150 joules. If that cardioversion is unsuccessful, then we would administer Amiodarone intravenously over a 20-minute period, and this can be then repeated over a 24-hour period whilst the patient is in specialist care.

And finally, to summarize the blood flow through the heart, we can see in the diagram blood enters the right side of the heart through the right atrium. This is deoxygenated blood, and is shown here in the diagram as blue. It passes through the atrioventricular valve into the ventricle, and then up through the pulmonary trunk through the pulmonary valve, and into the pulmonary circulation to be oxygenated in the lungs. We switch to the left-hand side of the heart now, and we can see blood returning back to the left atrium from the lungs via the pulmonary veins, passing through the atrioventricular valve into the left ventricle. The left ventricle fills, and when it contracts blood is passed through the aortic valve, through the aortic arch, and out to the systemic circulation. And we can see that this happens simultaneously on the left and the right side of the heart.

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