heartbeat too fast with congestive heart failure

Posted by corjianne @corjianne, Nov 19, 2017

I have CHF with an EF of 20 or so. Over the last few weeks, my doctor has told me my heart is beating too fast, about 100-150 bpm. He prescribed Digoxin, which gave me terrible stomach pains. Does anyone have an experience with this?
Thanks.

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I wish the patients who found successful medications to help high bpm would list these meds. Not to copy for all of us, but to help make our suggestions to our doctors. I was interested in Entresto. Thx.

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solatol and amlodipine works for me

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@oldkarl

@hopeful33250 Sure, Teresa. The nerve/muscle issue is not difficult to understand. Amyloidosis is a matter of genetically mis-formed protein particles. Form many people, this process begins at conception. For others, it is available, beginning at conception, but does not operate until triggered by something like radon, 2-4D, 2-4-5T, Roundup, radiation from nuclear testing, or some chemical. There are many triggers to actually start the protein to mis-form. In any case, the pieces of protein, usually produced by the liver, float around the body to do their necessary work. But the mis-formed pieces create more mis-formed pieces in the liver, but should be filtered out by the body, especially the kidneys. But the kidneys get plugged, so the pieces then deposit themselves in any tissue in the body. Nerve, muscle, bone, fat, whatever. Each mutation has its special place to deposit itself. Just like me cat has a special place it likes to sleep at night. Anyway, some forms are fibrilogenic, meaning they get into a tissue, then make little tubes of water called fibrils. These fibrils push the cells of the nerves and/or muscles apart, interrupting their ability to work. The muscles get weaker, not able to tense up. The sensori-motor nerves cannot pass the signals from the brain. So the heart cannot beat, the lungs can not breathe properly. The skin tissue is not able to reproduce itself smoothly and colored properly. Some dead protein is deposited in the bottom of the cerebellum, and is called Alzheimers. My form of dementia is deposited in the top of the cerebellum and is called cerebral cortex Amyloidosis. It all stems from mis-folded protein particles which float around the body. They are like several children's jacks laid out to make a layer of them, then another layer on top of the first can be laid down, but will only fit a certain way, and another, etc., until it makes a chain of protein. If they do not fit, one layer on another, the layers die, and form fibrils. So you get a test, developed by Bindings of UK, called "Serum FreeLiteChain@ Assay, and do a 24-hour Proteinuria assay, to discover whether your kidneys are filtering out all the misfolded or unused protein. If the sFLC number is 1.8 mg/dl, or the 24-hr Proteinuria is 0.500 G/24 hour, you have some form of Amyloidosis, and must be tested to determine the mutation of your over-abundant protein. I know this is a lot, but maybe it will help.

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@hopeful33250 Hi, Teresa. The DX for the particular form or forms of Amy that I have is always a work in progress. Since no certainty of biopsy exists for any form of hATTR, especially hATTRwt, the most certain tests are a combination of tests. My dX has come from the evidence of several tests, including the deaths of my sister and my niece and their post-mortem examinations, Serum protein Electrophoresis, Serum Immunofixation Electrophoresis, Serum FreeLiteChain(c), Urine Protein Electrophoresis. the sFLC and the 24-hr PEL and IFE together constitute, according to their maker, Bindings Site, a 100% certainty of diagnosis, although Medicare says they want a biopsy. All the details of the last table of my medical witness show the evidence, and the percentage of proven Amyloidosis patients who present these evidences. For instance, the sFLC of 1.8 or more is presented by 100% of known LiteChain patients. I will have to get a biopsy soon to finish the dX, biopsy probably of skin, kidney, liver, lymph, and perhaps others. Medicare is doing the best they can to avoid the dX, although it would save them money. Page 12 or so of my story at https://bit.Ly/1w7j4j8 has a discussion of some of the various mutations and what tests should show their presence. We all hope that Medicare will soon begin to trust the Bindings/Mayo dX pattern.

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@soloact

The Vagal maneuver is a known way that can stop a racing heartbeat, although medication might be necessary for long term, as others have said:

Vagal maneuver and Valsalva maneuver (options, not all 3):

Strain as if having a difficult bowel movement

Rub the neck just below the angle of the jaw (which stimulates a sensitive area on the carotid artery called the carotid sinus)

Plunge the face into a bowl of ice-cold water

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A cardiology nurse told me about it. She gets tachycardia, too. I have it intermittently.

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@leew1936

solatol and amlodipine works for me

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Thank you

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@oldkarl

@hopeful33250 Sure, Teresa. The nerve/muscle issue is not difficult to understand. Amyloidosis is a matter of genetically mis-formed protein particles. Form many people, this process begins at conception. For others, it is available, beginning at conception, but does not operate until triggered by something like radon, 2-4D, 2-4-5T, Roundup, radiation from nuclear testing, or some chemical. There are many triggers to actually start the protein to mis-form. In any case, the pieces of protein, usually produced by the liver, float around the body to do their necessary work. But the mis-formed pieces create more mis-formed pieces in the liver, but should be filtered out by the body, especially the kidneys. But the kidneys get plugged, so the pieces then deposit themselves in any tissue in the body. Nerve, muscle, bone, fat, whatever. Each mutation has its special place to deposit itself. Just like me cat has a special place it likes to sleep at night. Anyway, some forms are fibrilogenic, meaning they get into a tissue, then make little tubes of water called fibrils. These fibrils push the cells of the nerves and/or muscles apart, interrupting their ability to work. The muscles get weaker, not able to tense up. The sensori-motor nerves cannot pass the signals from the brain. So the heart cannot beat, the lungs can not breathe properly. The skin tissue is not able to reproduce itself smoothly and colored properly. Some dead protein is deposited in the bottom of the cerebellum, and is called Alzheimers. My form of dementia is deposited in the top of the cerebellum and is called cerebral cortex Amyloidosis. It all stems from mis-folded protein particles which float around the body. They are like several children's jacks laid out to make a layer of them, then another layer on top of the first can be laid down, but will only fit a certain way, and another, etc., until it makes a chain of protein. If they do not fit, one layer on another, the layers die, and form fibrils. So you get a test, developed by Bindings of UK, called "Serum FreeLiteChain@ Assay, and do a 24-hour Proteinuria assay, to discover whether your kidneys are filtering out all the misfolded or unused protein. If the sFLC number is 1.8 mg/dl, or the 24-hr Proteinuria is 0.500 G/24 hour, you have some form of Amyloidosis, and must be tested to determine the mutation of your over-abundant protein. I know this is a lot, but maybe it will help.

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Thank you @oldkarl, I'm looking forward to reading your story. How interesting!

Teresa

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@peach414144

yes , several years ago: my heart was beating at 130 or more when i was at rest. if this would continue then the heart would stiffen and an early death. the doctor prescribed three medications for the heart. it has been working now for about five years. i am eighty years of age and still feel well. each person is a different case so i do not think it would be wise to reveal the medications prescribed. perhaps a second opinion with a new doctor might be wise for your well being. take care of yourself and with love, peach barbara.

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For my congestive heart failure, my dosage of 1/2 of a 6.25 of carvedilol has been increased to a full 6.25 twice a day. My BP looks better, not perfect, and my heartbeat is a little less (under 95), but now my feet get very cold. Have I hurt my circulation by the increase in Carvedilol? Sounds silly but I am new at all this. I am 70. My mother died of congestive heart failure at 73. Her only medication was lasix. Arlene

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@corgianne Actually, what you describe is more like the walls of the heart have become thick (13-19) and leathery, forcing the heart to beat faster but less efficiently to pump the proper supply of blood. This is the result of Amyloid fibrils invading the muscles and nerves. Some folks say the shorted supply must be to my weak brain, but I just try to ignore them.

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>> walls of the heart have become thick (13-19) and leathery, forcing the heart to beat faster but less efficiently to pump the proper supply of blood.

Sounds like you're describing heart failure, and that happens most often simply because of old age. Our bodies wear out. That's why it's becoming more common. We live longer, so we end up with diseases related to the body starting to break down.

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@soloact

>> walls of the heart have become thick (13-19) and leathery, forcing the heart to beat faster but less efficiently to pump the proper supply of blood.

Sounds like you're describing heart failure, and that happens most often simply because of old age. Our bodies wear out. That's why it's becoming more common. We live longer, so we end up with diseases related to the body starting to break down.

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So the increased medication for the heart failure and resulting lower BP and pulse rate would not cause any change in circulation to my extremities, particularly my feet? Since I have diabetes (no neuropathy in feet), this concerned me.

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