Naked Science Forum
Life Sciences => Physiology & Medicine => Topic started by: Pseudoscience-is-malarkey on 28/10/2023 14:37:20
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These mega-expensive devices were all the rave for a very brief period of time, until researchers apparently saw unimpressive results, which caused both private and public healthcare entities to not pay for them.
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Apart from the problem of powering the device I think the main problem is the biocompatibility of the materials used. Most foreign materials will lead to clot formation requiring anticoagulant therapy with all the associated hazards. In addition how can an artificial deal with the changing circulation requirements of the body? Personally I think it's a dead end and the possibility of a replacement grown from one's stem cells, although not yet achievable, is the way to go.
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From a materials perspective, you have a constantly flexing component, 100,000 times a day.
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The materials problem can be circumvented in principle by using a brushless motor axial turbo pump. Total heart function has been replaced for short periods in animal experiments but it seems that pusatile flow is actually essential to prevent thrombus formation, and whilst a reversible axial turbo can achieve this in principle, it is difficult to prevent damage to the blood cells in contact with a hard edge. Such pumps are used for a short period as left ventricle assist devices to allow heart muscle recovery.
Powering a implanted pump is a nontrivial matter. FDA will not sanction percutaneous (plug and socket) connection for a permanent implant and transcutaneous (like a contactless phone charger) charging is still problematic. Although mechanical pumps are more efficient than the real thing, when I was involved in this work we were looking at a continuous 5 watt requirement. 50Wh is obtainable from reliable laptop batteries, and such a device could indeed be implanted, but we faced the same problem as battery-powered vehicles, only worse. You need to restrict your charging rate to prevent overheating - you don't want to raise the local temperature around the battery by more than a degree, or you will upset the body's thermoregulation and produce discomfort if not actual harm. But you don't want to tie your patient to the recharging point for more than, say, an hour per day, perhaps in two 30 minute sessions, so, allowing for battery inefficiency, and a margin of error (you don't want your patient to die because the bus was late) you need to transfer about 150W (no problem) without cooking the patient (problem!) The solution is to use a large receiver antenna so the power (i.e. heat) lost in the transmission process is distributed over a large area. And now we run into a mechanics and materials problem - human flesh is flexible and elastic: how do we implant a wire cage that doesn't impede movement or breathing, and won't tear into muscles or organs? Fortunately we have a large, rigid structure with a good blood flow - the head. So we might make a recharging helmet that supplies a coil buried under the scalp. Except that whilst the heart and contents of the chest cavity generally are fairly robust, doing extensive surgery around the head and neck (you need to connect the receiver coil to the battery) adds a lot of complications because of all the other rather critical "wiring" in the area. Maybe the pelvis, and a "hot seat"?
It's an intriguing prospect for the next generation of clinical engineers. Good luck!
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how can an artificial deal with the changing circulation requirements
That begs the question of how they reconnect the autonomic nervous system to a transplanted heart, which in turn begs the question how is your own heart controlled after the ANS has been disconnected by a pulmonary vein isolation.
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Not my area, but as far as know heart rhythm is controlled internally by the sinoatrial node with inhibitory input fro the vagus nerve.
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Not my area, but as far as know heart rhythm is controlled internally by the sinoatrial node with inhibitory input fro the vagus nerve.
I don't really see how the heart can know what rate is required without some information from outside though.
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The primary control inputs are the vagus nerve (slow down) and the sympathetic cardiac nerves (speed up or pump harder). My preference would be to leave the real heart in place and either run parallel leads from the nerves or detect the electrical activity of the heart itself in response to those inputs, and use that to get the machine to copy the heart beat - an extension of the demand pacemaker..
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Vhfpmr, the sino-atrial node(pacemaker) will pick up decreased oxygen levels when there is greater demand and increase the rate, the medics refer to this as it's chronotropic effect. As regards the force of contractions, called the inotropic effect, I can't remember offhand what the inputs are. Alan reckons it is sympathetic inputs and I would go with this. All of what I have said is simple outline and the control of this and most bodily functions is quite complex with multiple feedback loops.
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The primary control inputs are the vagus nerve (slow down) and the sympathetic cardiac nerves (speed up or pump harder). My preference would be to leave the real heart in place and either run parallel leads from the nerves or detect the electrical activity of the heart itself in response to those inputs, and use that to get the machine to copy the heart beat - an extension of the demand pacemaker..
That's how I understand it, but the parasympathetic (vagal) and sympathetic nerves are collectively the autonomic nervous system, which enters the heart at the pulmonary veins, and is isolated by ablation to treat atrial fibrillation.
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Don't they have pacemakers where you come from?
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Don't they have pacemakers where you come from?
Are you talking to me?
Pacemakers aren't used to treat AF except in extremis for intractable cases. Furthermore, ablate & pace doesn't actually stop the AF, it just kills the AV node to prevent the rogue electrical signals from passing though it to the ventricles and causing fast AF. Of all the punters on the AF forum (with an international clientele served by many different healthcare systems) I don't recall seeing anyone who had had their AF treated by ablate & pace, they were all treated with either antiarrhythmic drugs or PVI ablation. Insofar as it's done at all, it's rare.
The pulmonary veins are isolated to treat AF not because the veins cause the arrhythmia, but because that's the location where the autonomic nervous system enters the heart. Patients who have had their AF successfully controlled with a PVI are able to resume active life, even athletics at Olympic level, hence my curiosity as to how the heart can continue to respond effectively to workload.
Not my area, but as far as know heart rhythm is controlled internally by the sinoatrial node with inhibitory input from the vagus nerve.
The sinus node is the heart's natural pacemaker, but what's telling it what rate is required if not the ANS? It's quite a few years since I read about this now, but as I recall in vagal AF the arrhythmia appears when the parasympathetic NS slows the HR to the point where heart muscle cells fire by themselves prematurely, a bit like athletes jumping the gun. Conversely an AF episode can also be triggered when the sympathetic NS is stimulated, such as during exercise, which wouldn't be explained by the above mechanism.