Application Information

This drug has been submitted to the FDA under the reference 006327/002.

Names and composition

"ISUPREL" is the commercial name of a drug composed of ISOPROTERENOL HYDROCHLORIDE.

Forms

ApplId/ProductId Drug name Active ingredient Form Strenght
006327/002 ISUPREL ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.5%
006327/003 ISUPREL ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 1%
006328/001 ISUPREL ISOPROTERENOL HYDROCHLORIDE TABLET/RECTAL, SUBLINGUAL 10MG
006328/002 ISUPREL ISOPROTERENOL HYDROCHLORIDE TABLET/RECTAL, SUBLINGUAL 15MG
010515/001 ISUPREL ISOPROTERENOL HYDROCHLORIDE INJECTABLE/INJECTION 0.2MG per ML
011178/001 ISUPREL ISOPROTERENOL HYDROCHLORIDE AEROSOL, METERED/INHALATION 0.103MG per INH

Similar Active Ingredient

ApplId/ProductId Drug name Active ingredient Form Strenght
006327/002 ISUPREL ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.5%
006327/003 ISUPREL ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 1%
006328/001 ISUPREL ISOPROTERENOL HYDROCHLORIDE TABLET/RECTAL, SUBLINGUAL 10MG
006328/002 ISUPREL ISOPROTERENOL HYDROCHLORIDE TABLET/RECTAL, SUBLINGUAL 15MG
007245/001 AEROLONE ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.25%
010375/004 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE AEROSOL, METERED/INHALATION 0.12MG per INH
010515/001 ISUPREL ISOPROTERENOL HYDROCHLORIDE INJECTABLE/INJECTION 0.2MG per ML
011178/001 ISUPREL ISOPROTERENOL HYDROCHLORIDE AEROSOL, METERED/INHALATION 0.103MG per INH
016813/001 VAPO-ISO ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.5%
016814/001 NORISODRINE AEROTROL ISOPROTERENOL HYDROCHLORIDE DISC/INHALATION 0.25%
083283/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE INJECTABLE/INJECTION 0.02MG per ML
083346/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE INJECTABLE/INJECTION 0.2MG per ML
083431/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE INJECTABLE/INJECTION 0.2MG per ML
083486/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE INJECTABLE/INJECTION 0.2MG per ML
083724/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE INJECTABLE/INJECTION 0.2MG per ML
085540/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.5%
085904/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE AEROSOL, METERED/INHALATION 0.12MG per INH
085994/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.25%
086764/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.5%
087935/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.031%
087936/001 ISOPROTERENOL HYDROCHLORIDE ISOPROTERENOL HYDROCHLORIDE SOLUTION/INHALATION 0.062%

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Answered questions

Ml/hr (dosage/wt or BSA/hr or min prescribed)?
Isuprel is to be infused at a rate of 0.05mcg/kg/minute. 1mg of Isuprel has been added to destrose 5% water. The final solution has a total volume of 50ml. Your patients current weight is 22lbs. The IV should be infused at how many ml per hr? Asked by Loyce Swindoll 1 year ago.

1000 mcgs in 50 mls, turns out to be 30mcg per hour..i'm getting 1.2 mls per hour. Answered by Angelyn Tocci 1 year ago.


Drugs for bradycardia with symptoms?
What drugs does a nurse give to a patient when they are in symptomtic bradycardia? Asked by Neda Lackner 1 year ago.

In an emergency situation atropine,isuprel. Answered by Araceli Radmall 1 year ago.

I'm not sure what your question really is, but if you have ANY questions about bradycardia or its symptoms, you can go to www.webmd.com and search under bradycardia, symptoms or bradycardia, medications. WebMD is an outstanding, authoritative, reliable medical website. Answered by Ava Mangram 1 year ago.


Asthma results in the constriction of bronchioles. What chemical will reverse it?
Asked by Aimee Delellis 1 year ago.

All brochodilalators are derivative of epinephrine. They started by trying to limit the Beat 1 agonists with Isuprel. Then further refinement led to Bronkosol, Alupent and now Albuterol sulfate. This is a Beta 2 agonists with very few side effects that were seen with earlier preparations. But these are all bronchodilators, a muscle relaxant for the bronchial airway muscles. That's not the only cause of constriction though. You have to consider the inflammation and consequent swelling of the bronchial walls. Also increased production of thick viscous mucous is a major contributing factor. Answered by Gaylord Ruark 1 year ago.

Medications can reverse the constriction caused by asthma that in turn causes inflamed airways. There are several medications used to treat asthma: -Bronchodliators: these medications contain a drug that opens the airways and come in short-acting or long-acting forms. Short acting bronchodliators such as salbutamol/albuterol [Ventolin] are taken when symptoms occur and begin working immediately and peak within 5-15 minutes to relieve symptoms. Short acting bronchodilators are also used by many asthmatics before exercise to prevent exercise induced asthma flares. In asthma treatment, except for in mild intermittent asthma, controller medications are usually needed, and are taken daily. This is where long acting bronchodilators can come into play: Long-acting bronchodilators are used in combination with corticosteroids [Advair is a combination inhaler, Serevent just contains a long acting bronchodilator]. These peak within 15-20 minutes, and their effects last for 12 hours to control asthma symptoms. These should not be used during an asthma flare, that's what the short-acting bronchodilator is for. -Corticosteroids come in either an inhaled, oral or injected form, but for maintenance therapy typically are used in the inhaled form through a puffer or 'diskus' device. Examples of inhaled corticosteroids are FloVent, QVar, Alvesco and Symbicort. These are typically inhaled twice a day, except for Alvesco, which has once-daily dosing. Oral corticosteroids [Prednisone] contain much higher doses and have much higher risk for side effects than inhaled corticosteroids. They are typically used in asthma emergencies or to head off a serious asthma attack that's already started. Injected corticosteroids are typically used when a patient is unresponsive, undergoing respiratory distress, in an emergency situation to bring down serious inflammation in the airways. -Leukotriene receptor antagonists aka leukotriene modifiers are taken in pill form and work differently than corticosteroids to reduce inflammation in the airways. Leukotriene receptor antagonists [Singulair] work to block leukotrienes released in the airways that cause inflammation, specifically in allergic asthma. Leukotriene modifiers can also be taken 2 hours prior to exercise to prevent exercise induced asthma. Either an inhaled corticosteroid or a leukotriene modifier is first-line asthma controller treatment. If a person is using their fast-acting bronchodilator [ventolin] more than 3 times a week except for before exercise, they should be on a controller medication. If adequate control isn't achieved after adding an inhaled corticosteroid, a leukotriene modifier may be added, or vice versa. Next up is the long-acting bronchodilator, then, if need be and typically only in severe cases, oral corticosteroids to get a flare under control. Answered by Milo Kamal 1 year ago.

asthma results constriction bronchioles chemical reverse Answered by Mui Kuepfer 1 year ago.

The Chinese way of curing the asthma is to consume bird nest soup. For more detail please log on to www.qqbirdnest.com Answered by Luella Blinks 1 year ago.

Albuterol a bronchodilater. atrovent sometimes. albuterol is the emergency bronchodilater. Answered by Linnie Carback 1 year ago.


Will sympathomimetic drug help a person with asthma?
Asked by Violette Chaudhry 1 year ago.

A sympathomimetic drug is the bronchodilators doctors prescribe for people with asthma or conditions with asthmatic components to it. These include, Isuprel, Bronkosol, Alupent, Albuterol etc. The body has two systems of autonomic nerves. Sympathetic and the parasympathetic. Where one does one thing the other does the opposite. The term sympathomimetic means something that will "mimic" the sympathetic nervous system. Sympathomimetics dilate or relax the bronchial muscles so you can see it would be very useful in asthmatic patients. As I said there are two systems so another approach some doctors use is to give the patient a parasympatholytic medicine (Atrovent) to reduce the influence of the parasympathetic system.They will give a sympathomimetic and a parasympatholytic at the same time. God bless. Answered by Leeanna Utzig 1 year ago.

idk, do BITCHES EAT 'SCREAM? (ice cream) listen, dont ask on yahoo answers. no one here has a medical degree, save 1 or 2 Answered by Tula Moya 1 year ago.


Tilt Table Test (TTT)?
The hospital where I'm having it done uses the EP Lab and they do use Isuprel if necessary. That is the reason for my questions concerning arrhythmias. Asked by Glynda Overly 1 year ago.

I am scheduled for a TTT next Tuesday and I have a few questions. I am a 5'3, 110 pound female. I have PVCs (trigeminy and bigeminy), PACS, mitral valve prolapse, sinus bradycardia, sinus tachycardia, and a sinus arrhythmia. My EP attempted to do a PVC ablation on Monday, but when he got in he found that they originate in the left ventricle and he said it would pose too many risks because of my "small frame." I get lightheaded and dizzy multiple times each day. These episodes are tied to the PVC runs--an extended run of trigeminy or bigeminy always precedes the incidents of lightheadedness and full syncope. There may be an opportunity for a second EPS and an ablation at a larger facility (Cleveland Clinic) who would be able to use a smaller balloon. Because my EP could not do the ablation, he ordered a TTT just to make sure there isn't any autonomic dysfunction as well. My questions are as follows: 1. Will my electrophysiologist or some another physician be in the room during the test in case something happens? 2. Will they stop the test early if too much arrhythmia is present, or will they only stop it prematurely if I actually faint? 3. If my EP is not present during the test, will he receive a a report of the arrhythmias that occurred during the test, or will he only get a list of my blood pressure and heart rate at various points? 4. Must a person actually faint for them to have a positive TTT, or do those administering the test evaluate other symptoms that occurred as well? Thank you so much. Answered by Darwin Violet 1 year ago.

It is highly unlikely that a tilt table test will induce an irregular heart beat in you. All that is involved in a tilt table test is that a nurse checks your blood pressure and pulse with the table flat, then they elevate the head of the table and lower the foot of the table gradually, rechecking your blood pressure and pulse with the table at different angles. If your blood pressure drops too low or your heart rate rises too fast, then that is a positive TTT...there's no reason to push it further until you actually faint. Answered by Edyth Felde 1 year ago.

Vasovagal Syncope? Might be Carotid Sinus Syncope. Sounds love it might be triggered through Central Ischaemic reaction, that is the brains reaction to loss of blood to the mind. Maybe you've got a blockage? Answered by Hoyt Wiedeman 1 year ago.


PVCs - Where to go from here?
I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. ... Asked by Kandis Hudec 1 year ago.

I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. They have lasted as long as eight hours. I finally made an appointment with an electrophysiologist in Toledo in October because the palpitations, lightheadedness, fatigue, and shortness of breath were getting unmanageable. I do not smoke, take recreational drugs, drink caffeine or alcohol, or anything of that nature. After the results of a 30-day event monitor came back in early December, my EP ordered a stress test and a Holter. Fortunately for me, but unfortunately for diagnostic purposes, I ended up having an unusually good day in terms of symptoms when I had the Holter and it only showed 10,000 PVCs. That is still a fair number. At my next appointment, when my EP reviewed the Holter and the stress test and I let him know that my symptoms were getting worse, he said “I really need to get in there to see what’s going on.” He also said that he thought he could “find at least a few spots to ablate.” I asked him if he could tell which side the PVCs were coming from and he said he thought the left. Because I was hesitant to consent to the EPS and ablation at that point, he put me on 12.5 mg Toprol. I had to go off of it within three days because I could not tolerate it. I came to my next appointment with a list of questions about the ablation and I was prepared to consent. My EP walks into the room and says “I will only do it if you can’t live with the PVCs.” There were no other intervening tests that could account for his change in tone. Anyway, after going back and forth a few times I finally had the EPS on Monday, March 7. For whatever reason, there were no PVCs at baseline, so he had to induce them with Isuprel. He came out of the control center and told me that they were coming from the left side and that he was not going to do the ablation because it was pose “too much of a risk to inflate the balloon in someone with such a small frame.” He also let me know that they were “severely limited in what we can do because of your past paradoxical reaction to Versed.” He used Demerol instead which immediately suppressed the PVCs for the rest of the study. There may have been a few, but the Demerol definitely toned them down. Even after he decided not to do the ablation, he put one catheter in my right femoral vein and did the pacing and some other things. QUESTIONS: --I am the same size now as I was in December. As I related above, at that time my EP thought he could find at least a few spots to ablate and he thought they would be in the left ventricle. On Monday, he would not do the ablation because of the dangers inherent in left ventricle ablations in someone with a “small frame.” He is inconsistent and inconsistent about important things. It honestly seems like a situation where my case is too complex for him and their facility, but he does not want to admit it. My friends, many of who are in the medical field are encouraging me to seek a second opinion if not switch doctors completely. Based on the evidence, would you recommend this as well? I am only about two hours from the Cleveland Clinic and I know that they do pediatric ablations, so they would have a smaller balloon if that is needed. --I had a paradoxical reaction to Versed 11 years ago. On Monday, they used 75mg of Demerol and that immediately stopped the PVCs. Is it possible for a person to have a paradoxical reaction to a drug and then have them react normally to it years later? My EP made a huge deal of how important it was to use Versed. --My EP is now suddenly blaming all of my symptoms on the mitral valve prolapse. He said the MVP was “mild.” I may be missing something, but that does not make sense. Am I missing something? --My EP scheduled me for a TTT on Tuesday. Is there a doctor present for the test? I know they sometimes use Isuprel to increase the heart rate, and that would induce a long run of PVCs in me and possible fainting if I am tilted up on the table. I realize that the purpose of the test is to induce syncope, but because the arrhythmia is so frequent with me and I do have attendant symptoms it might be good if a medical professional were in the room just in case! Thank you Jenn Answered by Delphia Esparsen 1 year ago.

Except for the unpleasant symptoms that they cause, PVCs like you have are benign--if you were not aware of them (and many people have 10s of thousands of PVCs/day and don't know it), they could be completely ignored. But since yours are on the left side, there would be some risk in attempting an ablation, as clots can always form during that procedure, and the left ventricle sends its blood directly to the brain. Hence you would be risking a stroke to treat a benign condition. If that were to happen, your cardiologist would be subject to justifiable criticism for doing the procedure. That may be part of this reason for his hesitancy. Some comments: >I am assuming that your echocardiogram has shown normal heart function. >There is absolutely no evidence that MVP causes PVCs, and the old concept of "MVP syndrome" has been discredited for years. Its only importance is if it causes mitral regurgitation, which does not appear to be the case with you. >I am not an EP specialist, but my understanding of ablation is that it involves either freezing or burning (with a radio frequency current) the tissue that is generating the PVCs. It does not involve a balloon for the kind of procedure that you would need. (It can involve piercing a small hole in the septum between the right and left atria; possibly that could raise a concern in someone with a "small frame.") >I do not understand the reason for the TTT. It makes no sense to me, but then all I know about your case is your brief summary... >If Toprol is the only try at medical management that you've had, you should investigate other drugs. But in any case, it appears that you and your cardiologist are not a good match. Find someone else. Answered by Will Spoonamore 1 year ago.

conventional untimely ventricular contractions. %. originate whilst another part of the middle (in the ventricles) than it relatively is organic heartbeat inititator initiates a beat. Answered by Joanna Stepro 1 year ago.


Why does the bronchodilator exaggerate the tachycardia?
Asked by Wilburn Macnair 1 year ago.

Bronchodilators were originally alpha or beta agonists. The grandfather of all of them is epinephrine.(Norepinephrine was primarily an alpha agonist and used mostly to treat kids with Croup.) Both of which would relax the bronchial muscles but had the side effect of increasing the heart rate. Through research it was found the the beta receptors were of two types, Beta 1 and beta 2. Beta 1 increased the heart rate while beta 2 relaxed the bronchial muscles. The pharmaceutical companies further refined the epinephrine to stimulate only the beta 2 receptors. They also refined it to block the beta 1 effects becoming the class of drugs known as beta blockers.This was used in tachyarrythmnias. Isuprel was the first beta agonist and it was very effective and fast acting but there was still a lot of beta 1 activity. Then came Bronkosol(Isoetharine) which seemed to have solved the problem. Alupent was next. Finally Albuterol was introduced which had virtually no beta 1 activity. The onset of activity was longer(up to 5 min.) but the effect on heart rate was much less. Some people still get an increase in heart rate with Albuterol but the percentage is very small. You still have to monitor the patient for heart rate increase but the likelihood is much less. I should have explained at the beginning that there are two types of nerves in the peripheral nervous system. Sympathetic and parasympathetic. While one has one effect the other has the opposite effect. Epinepherine is a sympathomimetic or "mimics" the sympathetic nerves. A drug which stimulates the parasympathetic system would be a parasympathomimetic. Any drug that reduces the effect of one of these is said to "lyse" the effect. So a drug which reduced the parasympathetic system would be called a parasympatholytic. The sympathetic system dilates or relaxes the bronchial muscles and the parasympathetic system constricts them. If you were to give a sympathomimetic and a parasympatholytic at the same time you would be attacking the problem from two sides. Atrovent is a parasympatholytic drug often given with Albuterol and is called Combivent. Studies have shown that in certain patients the bronchodilator effect is enhanced by the addition of Atrovent. God bless. Answered by Tressa Secondo 1 year ago.

because it has beta 1 receptor effect at the heart...which when stimulated caused an increased in heart beat Answered by Ollie Croshaw 1 year ago.


Why should one use a bronchodilator before a corticosteroid?
A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first,... Asked by Neoma Perschbacher 1 year ago.

A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first, then the steroid inhaler. -Rekha, RN/BSN Answered by Nakesha Samayoa 1 year ago.

Bronchodilators work systemically. They have no local effect. It's absorbed into the mucosa and thereby the blood vessels. Don't forget it has to be absorbed through the mucous layer and then the inflamed mucosa before it gets anywhere near the bronchial musculature. And, being Beta 2 agonists they only relax the bronchial muscles. They do not relieve inflammation. The saline is a mucolytic and works faster and locally. Of course, this is when you are taking the unit dose. If you are using the metered dose inhaler (MDI) there is no saline so it's best to wait 5 minutes for the full effect before taking the steroid. Once you cough the mucous out the bronchodilator can get to the membrane and be absorbed into the circulation faster. It is doing no good being absorbed by the mucous itself. Albuterol is the chemical evolutionary end product of epinephrine for the relief of bronchospasm. Epinephrine, of course, has primarily beta 1 and beta 2 effects. and it's very fast acting but it only lasts for maybe an hour. Isuprel was the next step. It's onset of effect was about 2 minutes but it remained effective for about two hours and the dose, as with epinephrine, had to be titred to the patient's heart rate. Bronkosol was the next in line. It's peak effect was achieved in 3-4 minutes but only lasted 3 hours. Alupent was about the same. Albuterol achieves it's maximum effect in 5 minutes and lasts for about 4 hours. All these meds were created in an attempt to mitigate the cardiac side effects by making them less beta 1 and more beta 2 agonists. Norepinephrine is primarily an alpha agonist and used, in titred doses, for acute laryngotracheobronchitis in children providing a fast acting anti inflammatory. Now once the bronchodilator is absorbed you can get maximum penetration of the steroid for it's localized effect on the inflammation and swelling. Also, a good tip is, if you are ordered to take two puffs from the MDI, wait 5 minutes between puffs so you get maximum effect from the first puff and the second one will get deeper. I know it's hard to wait but I always told my patients this and they all remarked what a difference it makes. Answered by Kirby Rodi 1 year ago.

Because if you relax and open the airways first, then the steriod can better penetrate the lungs to reduce inflammation. Answered by Joshua Dautrich 1 year ago.

ASKED AND ANSWERED. THANKS FOR THE POINTS! Answered by Marco Penale 1 year ago.


Ml/hr (dosage/wt or BSA/hr or min prescribed)?
Isuprel is to be infused at a rate of 0.05mcg/kg/minute. 1mg of Isuprel has been added to destrose 5% water. The final solution has a total volume of 50ml. Your patients current weight is 22lbs. The IV should be infused at how many ml per hr? Asked by Vinnie Gebhardt 1 year ago.

1000 mcgs in 50 mls, turns out to be 30mcg per hour..i'm getting 1.2 mls per hour. Answered by Kaylene Ketchie 1 year ago.


Drugs for bradycardia with symptoms?
What drugs does a nurse give to a patient when they are in symptomtic bradycardia? Asked by Kasi Emigholz 1 year ago.

In an emergency situation atropine,isuprel. Answered by Jarrod Glahn 1 year ago.

I'm not sure what your question really is, but if you have ANY questions about bradycardia or its symptoms, you can go to www.webmd.com and search under bradycardia, symptoms or bradycardia, medications. WebMD is an outstanding, authoritative, reliable medical website. Answered by Terina Ayres 1 year ago.


Asthma results in the constriction of bronchioles. What chemical will reverse it?
Asked by Keshia Debrosse 1 year ago.

All brochodilalators are derivative of epinephrine. They started by trying to limit the Beat 1 agonists with Isuprel. Then further refinement led to Bronkosol, Alupent and now Albuterol sulfate. This is a Beta 2 agonists with very few side effects that were seen with earlier preparations. But these are all bronchodilators, a muscle relaxant for the bronchial airway muscles. That's not the only cause of constriction though. You have to consider the inflammation and consequent swelling of the bronchial walls. Also increased production of thick viscous mucous is a major contributing factor. Answered by Susanna Vaux 1 year ago.

Medications can reverse the constriction caused by asthma that in turn causes inflamed airways. There are several medications used to treat asthma: -Bronchodliators: these medications contain a drug that opens the airways and come in short-acting or long-acting forms. Short acting bronchodliators such as salbutamol/albuterol [Ventolin] are taken when symptoms occur and begin working immediately and peak within 5-15 minutes to relieve symptoms. Short acting bronchodilators are also used by many asthmatics before exercise to prevent exercise induced asthma flares. In asthma treatment, except for in mild intermittent asthma, controller medications are usually needed, and are taken daily. This is where long acting bronchodilators can come into play: Long-acting bronchodilators are used in combination with corticosteroids [Advair is a combination inhaler, Serevent just contains a long acting bronchodilator]. These peak within 15-20 minutes, and their effects last for 12 hours to control asthma symptoms. These should not be used during an asthma flare, that's what the short-acting bronchodilator is for. -Corticosteroids come in either an inhaled, oral or injected form, but for maintenance therapy typically are used in the inhaled form through a puffer or 'diskus' device. Examples of inhaled corticosteroids are FloVent, QVar, Alvesco and Symbicort. These are typically inhaled twice a day, except for Alvesco, which has once-daily dosing. Oral corticosteroids [Prednisone] contain much higher doses and have much higher risk for side effects than inhaled corticosteroids. They are typically used in asthma emergencies or to head off a serious asthma attack that's already started. Injected corticosteroids are typically used when a patient is unresponsive, undergoing respiratory distress, in an emergency situation to bring down serious inflammation in the airways. -Leukotriene receptor antagonists aka leukotriene modifiers are taken in pill form and work differently than corticosteroids to reduce inflammation in the airways. Leukotriene receptor antagonists [Singulair] work to block leukotrienes released in the airways that cause inflammation, specifically in allergic asthma. Leukotriene modifiers can also be taken 2 hours prior to exercise to prevent exercise induced asthma. Either an inhaled corticosteroid or a leukotriene modifier is first-line asthma controller treatment. If a person is using their fast-acting bronchodilator [ventolin] more than 3 times a week except for before exercise, they should be on a controller medication. If adequate control isn't achieved after adding an inhaled corticosteroid, a leukotriene modifier may be added, or vice versa. Next up is the long-acting bronchodilator, then, if need be and typically only in severe cases, oral corticosteroids to get a flare under control. Answered by Roger Hoots 1 year ago.

asthma results constriction bronchioles chemical reverse Answered by Rupert Toxey 1 year ago.

The Chinese way of curing the asthma is to consume bird nest soup. For more detail please log on to www.qqbirdnest.com Answered by Flor Sub 1 year ago.

Albuterol a bronchodilater. atrovent sometimes. albuterol is the emergency bronchodilater. Answered by Leonor Fonesca 1 year ago.


Will sympathomimetic drug help a person with asthma?
Asked by Lawana Almasi 1 year ago.

A sympathomimetic drug is the bronchodilators doctors prescribe for people with asthma or conditions with asthmatic components to it. These include, Isuprel, Bronkosol, Alupent, Albuterol etc. The body has two systems of autonomic nerves. Sympathetic and the parasympathetic. Where one does one thing the other does the opposite. The term sympathomimetic means something that will "mimic" the sympathetic nervous system. Sympathomimetics dilate or relax the bronchial muscles so you can see it would be very useful in asthmatic patients. As I said there are two systems so another approach some doctors use is to give the patient a parasympatholytic medicine (Atrovent) to reduce the influence of the parasympathetic system.They will give a sympathomimetic and a parasympatholytic at the same time. God bless. Answered by Sharen Piechoski 1 year ago.

idk, do BITCHES EAT 'SCREAM? (ice cream) listen, dont ask on yahoo answers. no one here has a medical degree, save 1 or 2 Answered by Keith Morlino 1 year ago.


Tilt Table Test (TTT)?
The hospital where I'm having it done uses the EP Lab and they do use Isuprel if necessary. That is the reason for my questions concerning arrhythmias. Asked by Tanesha Gilhuly 1 year ago.

I am scheduled for a TTT next Tuesday and I have a few questions. I am a 5'3, 110 pound female. I have PVCs (trigeminy and bigeminy), PACS, mitral valve prolapse, sinus bradycardia, sinus tachycardia, and a sinus arrhythmia. My EP attempted to do a PVC ablation on Monday, but when he got in he found that they originate in the left ventricle and he said it would pose too many risks because of my "small frame." I get lightheaded and dizzy multiple times each day. These episodes are tied to the PVC runs--an extended run of trigeminy or bigeminy always precedes the incidents of lightheadedness and full syncope. There may be an opportunity for a second EPS and an ablation at a larger facility (Cleveland Clinic) who would be able to use a smaller balloon. Because my EP could not do the ablation, he ordered a TTT just to make sure there isn't any autonomic dysfunction as well. My questions are as follows: 1. Will my electrophysiologist or some another physician be in the room during the test in case something happens? 2. Will they stop the test early if too much arrhythmia is present, or will they only stop it prematurely if I actually faint? 3. If my EP is not present during the test, will he receive a a report of the arrhythmias that occurred during the test, or will he only get a list of my blood pressure and heart rate at various points? 4. Must a person actually faint for them to have a positive TTT, or do those administering the test evaluate other symptoms that occurred as well? Thank you so much. Answered by Aron Slaight 1 year ago.

It is highly unlikely that a tilt table test will induce an irregular heart beat in you. All that is involved in a tilt table test is that a nurse checks your blood pressure and pulse with the table flat, then they elevate the head of the table and lower the foot of the table gradually, rechecking your blood pressure and pulse with the table at different angles. If your blood pressure drops too low or your heart rate rises too fast, then that is a positive TTT...there's no reason to push it further until you actually faint. Answered by Carlton Pyke 1 year ago.

Vasovagal Syncope? Might be Carotid Sinus Syncope. Sounds love it might be triggered through Central Ischaemic reaction, that is the brains reaction to loss of blood to the mind. Maybe you've got a blockage? Answered by Wesley Lemarie 1 year ago.


PVCs - Where to go from here?
I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. ... Asked by Billie Matesic 1 year ago.

I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. They have lasted as long as eight hours. I finally made an appointment with an electrophysiologist in Toledo in October because the palpitations, lightheadedness, fatigue, and shortness of breath were getting unmanageable. I do not smoke, take recreational drugs, drink caffeine or alcohol, or anything of that nature. After the results of a 30-day event monitor came back in early December, my EP ordered a stress test and a Holter. Fortunately for me, but unfortunately for diagnostic purposes, I ended up having an unusually good day in terms of symptoms when I had the Holter and it only showed 10,000 PVCs. That is still a fair number. At my next appointment, when my EP reviewed the Holter and the stress test and I let him know that my symptoms were getting worse, he said “I really need to get in there to see what’s going on.” He also said that he thought he could “find at least a few spots to ablate.” I asked him if he could tell which side the PVCs were coming from and he said he thought the left. Because I was hesitant to consent to the EPS and ablation at that point, he put me on 12.5 mg Toprol. I had to go off of it within three days because I could not tolerate it. I came to my next appointment with a list of questions about the ablation and I was prepared to consent. My EP walks into the room and says “I will only do it if you can’t live with the PVCs.” There were no other intervening tests that could account for his change in tone. Anyway, after going back and forth a few times I finally had the EPS on Monday, March 7. For whatever reason, there were no PVCs at baseline, so he had to induce them with Isuprel. He came out of the control center and told me that they were coming from the left side and that he was not going to do the ablation because it was pose “too much of a risk to inflate the balloon in someone with such a small frame.” He also let me know that they were “severely limited in what we can do because of your past paradoxical reaction to Versed.” He used Demerol instead which immediately suppressed the PVCs for the rest of the study. There may have been a few, but the Demerol definitely toned them down. Even after he decided not to do the ablation, he put one catheter in my right femoral vein and did the pacing and some other things. QUESTIONS: --I am the same size now as I was in December. As I related above, at that time my EP thought he could find at least a few spots to ablate and he thought they would be in the left ventricle. On Monday, he would not do the ablation because of the dangers inherent in left ventricle ablations in someone with a “small frame.” He is inconsistent and inconsistent about important things. It honestly seems like a situation where my case is too complex for him and their facility, but he does not want to admit it. My friends, many of who are in the medical field are encouraging me to seek a second opinion if not switch doctors completely. Based on the evidence, would you recommend this as well? I am only about two hours from the Cleveland Clinic and I know that they do pediatric ablations, so they would have a smaller balloon if that is needed. --I had a paradoxical reaction to Versed 11 years ago. On Monday, they used 75mg of Demerol and that immediately stopped the PVCs. Is it possible for a person to have a paradoxical reaction to a drug and then have them react normally to it years later? My EP made a huge deal of how important it was to use Versed. --My EP is now suddenly blaming all of my symptoms on the mitral valve prolapse. He said the MVP was “mild.” I may be missing something, but that does not make sense. Am I missing something? --My EP scheduled me for a TTT on Tuesday. Is there a doctor present for the test? I know they sometimes use Isuprel to increase the heart rate, and that would induce a long run of PVCs in me and possible fainting if I am tilted up on the table. I realize that the purpose of the test is to induce syncope, but because the arrhythmia is so frequent with me and I do have attendant symptoms it might be good if a medical professional were in the room just in case! Thank you Jenn Answered by Elliott Obeng 1 year ago.

Except for the unpleasant symptoms that they cause, PVCs like you have are benign--if you were not aware of them (and many people have 10s of thousands of PVCs/day and don't know it), they could be completely ignored. But since yours are on the left side, there would be some risk in attempting an ablation, as clots can always form during that procedure, and the left ventricle sends its blood directly to the brain. Hence you would be risking a stroke to treat a benign condition. If that were to happen, your cardiologist would be subject to justifiable criticism for doing the procedure. That may be part of this reason for his hesitancy. Some comments: >I am assuming that your echocardiogram has shown normal heart function. >There is absolutely no evidence that MVP causes PVCs, and the old concept of "MVP syndrome" has been discredited for years. Its only importance is if it causes mitral regurgitation, which does not appear to be the case with you. >I am not an EP specialist, but my understanding of ablation is that it involves either freezing or burning (with a radio frequency current) the tissue that is generating the PVCs. It does not involve a balloon for the kind of procedure that you would need. (It can involve piercing a small hole in the septum between the right and left atria; possibly that could raise a concern in someone with a "small frame.") >I do not understand the reason for the TTT. It makes no sense to me, but then all I know about your case is your brief summary... >If Toprol is the only try at medical management that you've had, you should investigate other drugs. But in any case, it appears that you and your cardiologist are not a good match. Find someone else. Answered by Xiao Demny 1 year ago.

conventional untimely ventricular contractions. %. originate whilst another part of the middle (in the ventricles) than it relatively is organic heartbeat inititator initiates a beat. Answered by Alfreda Ragsdale 1 year ago.


Why does the bronchodilator exaggerate the tachycardia?
Asked by Hans Perrigo 1 year ago.

Bronchodilators were originally alpha or beta agonists. The grandfather of all of them is epinephrine.(Norepinephrine was primarily an alpha agonist and used mostly to treat kids with Croup.) Both of which would relax the bronchial muscles but had the side effect of increasing the heart rate. Through research it was found the the beta receptors were of two types, Beta 1 and beta 2. Beta 1 increased the heart rate while beta 2 relaxed the bronchial muscles. The pharmaceutical companies further refined the epinephrine to stimulate only the beta 2 receptors. They also refined it to block the beta 1 effects becoming the class of drugs known as beta blockers.This was used in tachyarrythmnias. Isuprel was the first beta agonist and it was very effective and fast acting but there was still a lot of beta 1 activity. Then came Bronkosol(Isoetharine) which seemed to have solved the problem. Alupent was next. Finally Albuterol was introduced which had virtually no beta 1 activity. The onset of activity was longer(up to 5 min.) but the effect on heart rate was much less. Some people still get an increase in heart rate with Albuterol but the percentage is very small. You still have to monitor the patient for heart rate increase but the likelihood is much less. I should have explained at the beginning that there are two types of nerves in the peripheral nervous system. Sympathetic and parasympathetic. While one has one effect the other has the opposite effect. Epinepherine is a sympathomimetic or "mimics" the sympathetic nerves. A drug which stimulates the parasympathetic system would be a parasympathomimetic. Any drug that reduces the effect of one of these is said to "lyse" the effect. So a drug which reduced the parasympathetic system would be called a parasympatholytic. The sympathetic system dilates or relaxes the bronchial muscles and the parasympathetic system constricts them. If you were to give a sympathomimetic and a parasympatholytic at the same time you would be attacking the problem from two sides. Atrovent is a parasympatholytic drug often given with Albuterol and is called Combivent. Studies have shown that in certain patients the bronchodilator effect is enhanced by the addition of Atrovent. God bless. Answered by Dortha Shaver 1 year ago.

because it has beta 1 receptor effect at the heart...which when stimulated caused an increased in heart beat Answered by Lynetta Schaubert 1 year ago.


Why should one use a bronchodilator before a corticosteroid?
A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first,... Asked by Collen Lanosga 1 year ago.

A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first, then the steroid inhaler. -Rekha, RN/BSN Answered by Anabel Wilhelm 1 year ago.

Bronchodilators work systemically. They have no local effect. It's absorbed into the mucosa and thereby the blood vessels. Don't forget it has to be absorbed through the mucous layer and then the inflamed mucosa before it gets anywhere near the bronchial musculature. And, being Beta 2 agonists they only relax the bronchial muscles. They do not relieve inflammation. The saline is a mucolytic and works faster and locally. Of course, this is when you are taking the unit dose. If you are using the metered dose inhaler (MDI) there is no saline so it's best to wait 5 minutes for the full effect before taking the steroid. Once you cough the mucous out the bronchodilator can get to the membrane and be absorbed into the circulation faster. It is doing no good being absorbed by the mucous itself. Albuterol is the chemical evolutionary end product of epinephrine for the relief of bronchospasm. Epinephrine, of course, has primarily beta 1 and beta 2 effects. and it's very fast acting but it only lasts for maybe an hour. Isuprel was the next step. It's onset of effect was about 2 minutes but it remained effective for about two hours and the dose, as with epinephrine, had to be titred to the patient's heart rate. Bronkosol was the next in line. It's peak effect was achieved in 3-4 minutes but only lasted 3 hours. Alupent was about the same. Albuterol achieves it's maximum effect in 5 minutes and lasts for about 4 hours. All these meds were created in an attempt to mitigate the cardiac side effects by making them less beta 1 and more beta 2 agonists. Norepinephrine is primarily an alpha agonist and used, in titred doses, for acute laryngotracheobronchitis in children providing a fast acting anti inflammatory. Now once the bronchodilator is absorbed you can get maximum penetration of the steroid for it's localized effect on the inflammation and swelling. Also, a good tip is, if you are ordered to take two puffs from the MDI, wait 5 minutes between puffs so you get maximum effect from the first puff and the second one will get deeper. I know it's hard to wait but I always told my patients this and they all remarked what a difference it makes. Answered by Lilliam Waterworth 1 year ago.

Because if you relax and open the airways first, then the steriod can better penetrate the lungs to reduce inflammation. Answered by Jacki Wittel 1 year ago.

ASKED AND ANSWERED. THANKS FOR THE POINTS! Answered by Jimmie Bertholf 1 year ago.


Ml/hr (dosage/wt or BSA/hr or min prescribed)?
Isuprel is to be infused at a rate of 0.05mcg/kg/minute. 1mg of Isuprel has been added to destrose 5% water. The final solution has a total volume of 50ml. Your patients current weight is 22lbs. The IV should be infused at how many ml per hr? Asked by Temika Nonnemacher 1 year ago.

1000 mcgs in 50 mls, turns out to be 30mcg per hour..i'm getting 1.2 mls per hour. Answered by Lashaun Shakespeare 1 year ago.


Drugs for bradycardia with symptoms?
What drugs does a nurse give to a patient when they are in symptomtic bradycardia? Asked by Josette Szaflarski 1 year ago.

In an emergency situation atropine,isuprel. Answered by Brigette Tomaino 1 year ago.

I'm not sure what your question really is, but if you have ANY questions about bradycardia or its symptoms, you can go to www.webmd.com and search under bradycardia, symptoms or bradycardia, medications. WebMD is an outstanding, authoritative, reliable medical website. Answered by Alphonso Leake 1 year ago.


Asthma results in the constriction of bronchioles. What chemical will reverse it?
Asked by Malik Broch 1 year ago.

All brochodilalators are derivative of epinephrine. They started by trying to limit the Beat 1 agonists with Isuprel. Then further refinement led to Bronkosol, Alupent and now Albuterol sulfate. This is a Beta 2 agonists with very few side effects that were seen with earlier preparations. But these are all bronchodilators, a muscle relaxant for the bronchial airway muscles. That's not the only cause of constriction though. You have to consider the inflammation and consequent swelling of the bronchial walls. Also increased production of thick viscous mucous is a major contributing factor. Answered by Maritza Gramacy 1 year ago.

Medications can reverse the constriction caused by asthma that in turn causes inflamed airways. There are several medications used to treat asthma: -Bronchodliators: these medications contain a drug that opens the airways and come in short-acting or long-acting forms. Short acting bronchodliators such as salbutamol/albuterol [Ventolin] are taken when symptoms occur and begin working immediately and peak within 5-15 minutes to relieve symptoms. Short acting bronchodilators are also used by many asthmatics before exercise to prevent exercise induced asthma flares. In asthma treatment, except for in mild intermittent asthma, controller medications are usually needed, and are taken daily. This is where long acting bronchodilators can come into play: Long-acting bronchodilators are used in combination with corticosteroids [Advair is a combination inhaler, Serevent just contains a long acting bronchodilator]. These peak within 15-20 minutes, and their effects last for 12 hours to control asthma symptoms. These should not be used during an asthma flare, that's what the short-acting bronchodilator is for. -Corticosteroids come in either an inhaled, oral or injected form, but for maintenance therapy typically are used in the inhaled form through a puffer or 'diskus' device. Examples of inhaled corticosteroids are FloVent, QVar, Alvesco and Symbicort. These are typically inhaled twice a day, except for Alvesco, which has once-daily dosing. Oral corticosteroids [Prednisone] contain much higher doses and have much higher risk for side effects than inhaled corticosteroids. They are typically used in asthma emergencies or to head off a serious asthma attack that's already started. Injected corticosteroids are typically used when a patient is unresponsive, undergoing respiratory distress, in an emergency situation to bring down serious inflammation in the airways. -Leukotriene receptor antagonists aka leukotriene modifiers are taken in pill form and work differently than corticosteroids to reduce inflammation in the airways. Leukotriene receptor antagonists [Singulair] work to block leukotrienes released in the airways that cause inflammation, specifically in allergic asthma. Leukotriene modifiers can also be taken 2 hours prior to exercise to prevent exercise induced asthma. Either an inhaled corticosteroid or a leukotriene modifier is first-line asthma controller treatment. If a person is using their fast-acting bronchodilator [ventolin] more than 3 times a week except for before exercise, they should be on a controller medication. If adequate control isn't achieved after adding an inhaled corticosteroid, a leukotriene modifier may be added, or vice versa. Next up is the long-acting bronchodilator, then, if need be and typically only in severe cases, oral corticosteroids to get a flare under control. Answered by Lida Litz 1 year ago.

asthma results constriction bronchioles chemical reverse Answered by Liberty Berdine 1 year ago.

The Chinese way of curing the asthma is to consume bird nest soup. For more detail please log on to www.qqbirdnest.com Answered by Creola Winton 1 year ago.

Albuterol a bronchodilater. atrovent sometimes. albuterol is the emergency bronchodilater. Answered by Keesha Blatti 1 year ago.


Will sympathomimetic drug help a person with asthma?
Asked by Mirtha Kettle 1 year ago.

A sympathomimetic drug is the bronchodilators doctors prescribe for people with asthma or conditions with asthmatic components to it. These include, Isuprel, Bronkosol, Alupent, Albuterol etc. The body has two systems of autonomic nerves. Sympathetic and the parasympathetic. Where one does one thing the other does the opposite. The term sympathomimetic means something that will "mimic" the sympathetic nervous system. Sympathomimetics dilate or relax the bronchial muscles so you can see it would be very useful in asthmatic patients. As I said there are two systems so another approach some doctors use is to give the patient a parasympatholytic medicine (Atrovent) to reduce the influence of the parasympathetic system.They will give a sympathomimetic and a parasympatholytic at the same time. God bless. Answered by Ladawn Mccandles 1 year ago.

idk, do BITCHES EAT 'SCREAM? (ice cream) listen, dont ask on yahoo answers. no one here has a medical degree, save 1 or 2 Answered by Carina Sensabaugh 1 year ago.


Tilt Table Test (TTT)?
The hospital where I'm having it done uses the EP Lab and they do use Isuprel if necessary. That is the reason for my questions concerning arrhythmias. Asked by Gaynelle Lippard 1 year ago.

I am scheduled for a TTT next Tuesday and I have a few questions. I am a 5'3, 110 pound female. I have PVCs (trigeminy and bigeminy), PACS, mitral valve prolapse, sinus bradycardia, sinus tachycardia, and a sinus arrhythmia. My EP attempted to do a PVC ablation on Monday, but when he got in he found that they originate in the left ventricle and he said it would pose too many risks because of my "small frame." I get lightheaded and dizzy multiple times each day. These episodes are tied to the PVC runs--an extended run of trigeminy or bigeminy always precedes the incidents of lightheadedness and full syncope. There may be an opportunity for a second EPS and an ablation at a larger facility (Cleveland Clinic) who would be able to use a smaller balloon. Because my EP could not do the ablation, he ordered a TTT just to make sure there isn't any autonomic dysfunction as well. My questions are as follows: 1. Will my electrophysiologist or some another physician be in the room during the test in case something happens? 2. Will they stop the test early if too much arrhythmia is present, or will they only stop it prematurely if I actually faint? 3. If my EP is not present during the test, will he receive a a report of the arrhythmias that occurred during the test, or will he only get a list of my blood pressure and heart rate at various points? 4. Must a person actually faint for them to have a positive TTT, or do those administering the test evaluate other symptoms that occurred as well? Thank you so much. Answered by Daria Rengel 1 year ago.

It is highly unlikely that a tilt table test will induce an irregular heart beat in you. All that is involved in a tilt table test is that a nurse checks your blood pressure and pulse with the table flat, then they elevate the head of the table and lower the foot of the table gradually, rechecking your blood pressure and pulse with the table at different angles. If your blood pressure drops too low or your heart rate rises too fast, then that is a positive TTT...there's no reason to push it further until you actually faint. Answered by Napoleon Hefferon 1 year ago.

Vasovagal Syncope? Might be Carotid Sinus Syncope. Sounds love it might be triggered through Central Ischaemic reaction, that is the brains reaction to loss of blood to the mind. Maybe you've got a blockage? Answered by Elene Waynick 1 year ago.


PVCs - Where to go from here?
I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. ... Asked by Brigida Hallinger 1 year ago.

I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. They have lasted as long as eight hours. I finally made an appointment with an electrophysiologist in Toledo in October because the palpitations, lightheadedness, fatigue, and shortness of breath were getting unmanageable. I do not smoke, take recreational drugs, drink caffeine or alcohol, or anything of that nature. After the results of a 30-day event monitor came back in early December, my EP ordered a stress test and a Holter. Fortunately for me, but unfortunately for diagnostic purposes, I ended up having an unusually good day in terms of symptoms when I had the Holter and it only showed 10,000 PVCs. That is still a fair number. At my next appointment, when my EP reviewed the Holter and the stress test and I let him know that my symptoms were getting worse, he said “I really need to get in there to see what’s going on.” He also said that he thought he could “find at least a few spots to ablate.” I asked him if he could tell which side the PVCs were coming from and he said he thought the left. Because I was hesitant to consent to the EPS and ablation at that point, he put me on 12.5 mg Toprol. I had to go off of it within three days because I could not tolerate it. I came to my next appointment with a list of questions about the ablation and I was prepared to consent. My EP walks into the room and says “I will only do it if you can’t live with the PVCs.” There were no other intervening tests that could account for his change in tone. Anyway, after going back and forth a few times I finally had the EPS on Monday, March 7. For whatever reason, there were no PVCs at baseline, so he had to induce them with Isuprel. He came out of the control center and told me that they were coming from the left side and that he was not going to do the ablation because it was pose “too much of a risk to inflate the balloon in someone with such a small frame.” He also let me know that they were “severely limited in what we can do because of your past paradoxical reaction to Versed.” He used Demerol instead which immediately suppressed the PVCs for the rest of the study. There may have been a few, but the Demerol definitely toned them down. Even after he decided not to do the ablation, he put one catheter in my right femoral vein and did the pacing and some other things. QUESTIONS: --I am the same size now as I was in December. As I related above, at that time my EP thought he could find at least a few spots to ablate and he thought they would be in the left ventricle. On Monday, he would not do the ablation because of the dangers inherent in left ventricle ablations in someone with a “small frame.” He is inconsistent and inconsistent about important things. It honestly seems like a situation where my case is too complex for him and their facility, but he does not want to admit it. My friends, many of who are in the medical field are encouraging me to seek a second opinion if not switch doctors completely. Based on the evidence, would you recommend this as well? I am only about two hours from the Cleveland Clinic and I know that they do pediatric ablations, so they would have a smaller balloon if that is needed. --I had a paradoxical reaction to Versed 11 years ago. On Monday, they used 75mg of Demerol and that immediately stopped the PVCs. Is it possible for a person to have a paradoxical reaction to a drug and then have them react normally to it years later? My EP made a huge deal of how important it was to use Versed. --My EP is now suddenly blaming all of my symptoms on the mitral valve prolapse. He said the MVP was “mild.” I may be missing something, but that does not make sense. Am I missing something? --My EP scheduled me for a TTT on Tuesday. Is there a doctor present for the test? I know they sometimes use Isuprel to increase the heart rate, and that would induce a long run of PVCs in me and possible fainting if I am tilted up on the table. I realize that the purpose of the test is to induce syncope, but because the arrhythmia is so frequent with me and I do have attendant symptoms it might be good if a medical professional were in the room just in case! Thank you Jenn Answered by Deb Pyron 1 year ago.

Except for the unpleasant symptoms that they cause, PVCs like you have are benign--if you were not aware of them (and many people have 10s of thousands of PVCs/day and don't know it), they could be completely ignored. But since yours are on the left side, there would be some risk in attempting an ablation, as clots can always form during that procedure, and the left ventricle sends its blood directly to the brain. Hence you would be risking a stroke to treat a benign condition. If that were to happen, your cardiologist would be subject to justifiable criticism for doing the procedure. That may be part of this reason for his hesitancy. Some comments: >I am assuming that your echocardiogram has shown normal heart function. >There is absolutely no evidence that MVP causes PVCs, and the old concept of "MVP syndrome" has been discredited for years. Its only importance is if it causes mitral regurgitation, which does not appear to be the case with you. >I am not an EP specialist, but my understanding of ablation is that it involves either freezing or burning (with a radio frequency current) the tissue that is generating the PVCs. It does not involve a balloon for the kind of procedure that you would need. (It can involve piercing a small hole in the septum between the right and left atria; possibly that could raise a concern in someone with a "small frame.") >I do not understand the reason for the TTT. It makes no sense to me, but then all I know about your case is your brief summary... >If Toprol is the only try at medical management that you've had, you should investigate other drugs. But in any case, it appears that you and your cardiologist are not a good match. Find someone else. Answered by Paris Derego 1 year ago.

conventional untimely ventricular contractions. %. originate whilst another part of the middle (in the ventricles) than it relatively is organic heartbeat inititator initiates a beat. Answered by Claretha Solima 1 year ago.


Why does the bronchodilator exaggerate the tachycardia?
Asked by Jolynn Preus 1 year ago.

Bronchodilators were originally alpha or beta agonists. The grandfather of all of them is epinephrine.(Norepinephrine was primarily an alpha agonist and used mostly to treat kids with Croup.) Both of which would relax the bronchial muscles but had the side effect of increasing the heart rate. Through research it was found the the beta receptors were of two types, Beta 1 and beta 2. Beta 1 increased the heart rate while beta 2 relaxed the bronchial muscles. The pharmaceutical companies further refined the epinephrine to stimulate only the beta 2 receptors. They also refined it to block the beta 1 effects becoming the class of drugs known as beta blockers.This was used in tachyarrythmnias. Isuprel was the first beta agonist and it was very effective and fast acting but there was still a lot of beta 1 activity. Then came Bronkosol(Isoetharine) which seemed to have solved the problem. Alupent was next. Finally Albuterol was introduced which had virtually no beta 1 activity. The onset of activity was longer(up to 5 min.) but the effect on heart rate was much less. Some people still get an increase in heart rate with Albuterol but the percentage is very small. You still have to monitor the patient for heart rate increase but the likelihood is much less. I should have explained at the beginning that there are two types of nerves in the peripheral nervous system. Sympathetic and parasympathetic. While one has one effect the other has the opposite effect. Epinepherine is a sympathomimetic or "mimics" the sympathetic nerves. A drug which stimulates the parasympathetic system would be a parasympathomimetic. Any drug that reduces the effect of one of these is said to "lyse" the effect. So a drug which reduced the parasympathetic system would be called a parasympatholytic. The sympathetic system dilates or relaxes the bronchial muscles and the parasympathetic system constricts them. If you were to give a sympathomimetic and a parasympatholytic at the same time you would be attacking the problem from two sides. Atrovent is a parasympatholytic drug often given with Albuterol and is called Combivent. Studies have shown that in certain patients the bronchodilator effect is enhanced by the addition of Atrovent. God bless. Answered by Zoila Bowdich 1 year ago.

because it has beta 1 receptor effect at the heart...which when stimulated caused an increased in heart beat Answered by Joseph Hardney 1 year ago.


Why should one use a bronchodilator before a corticosteroid?
A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first,... Asked by Natosha Talamas 1 year ago.

A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first, then the steroid inhaler. -Rekha, RN/BSN Answered by Kristie Varone 1 year ago.

Bronchodilators work systemically. They have no local effect. It's absorbed into the mucosa and thereby the blood vessels. Don't forget it has to be absorbed through the mucous layer and then the inflamed mucosa before it gets anywhere near the bronchial musculature. And, being Beta 2 agonists they only relax the bronchial muscles. They do not relieve inflammation. The saline is a mucolytic and works faster and locally. Of course, this is when you are taking the unit dose. If you are using the metered dose inhaler (MDI) there is no saline so it's best to wait 5 minutes for the full effect before taking the steroid. Once you cough the mucous out the bronchodilator can get to the membrane and be absorbed into the circulation faster. It is doing no good being absorbed by the mucous itself. Albuterol is the chemical evolutionary end product of epinephrine for the relief of bronchospasm. Epinephrine, of course, has primarily beta 1 and beta 2 effects. and it's very fast acting but it only lasts for maybe an hour. Isuprel was the next step. It's onset of effect was about 2 minutes but it remained effective for about two hours and the dose, as with epinephrine, had to be titred to the patient's heart rate. Bronkosol was the next in line. It's peak effect was achieved in 3-4 minutes but only lasted 3 hours. Alupent was about the same. Albuterol achieves it's maximum effect in 5 minutes and lasts for about 4 hours. All these meds were created in an attempt to mitigate the cardiac side effects by making them less beta 1 and more beta 2 agonists. Norepinephrine is primarily an alpha agonist and used, in titred doses, for acute laryngotracheobronchitis in children providing a fast acting anti inflammatory. Now once the bronchodilator is absorbed you can get maximum penetration of the steroid for it's localized effect on the inflammation and swelling. Also, a good tip is, if you are ordered to take two puffs from the MDI, wait 5 minutes between puffs so you get maximum effect from the first puff and the second one will get deeper. I know it's hard to wait but I always told my patients this and they all remarked what a difference it makes. Answered by Leida Pash 1 year ago.

Because if you relax and open the airways first, then the steriod can better penetrate the lungs to reduce inflammation. Answered by Merrill Srinivasan 1 year ago.

ASKED AND ANSWERED. THANKS FOR THE POINTS! Answered by Tawana Weigelt 1 year ago.


Ml/hr (dosage/wt or BSA/hr or min prescribed)?
Isuprel is to be infused at a rate of 0.05mcg/kg/minute. 1mg of Isuprel has been added to destrose 5% water. The final solution has a total volume of 50ml. Your patients current weight is 22lbs. The IV should be infused at how many ml per hr? Asked by Ileana Hui 1 year ago.

1000 mcgs in 50 mls, turns out to be 30mcg per hour..i'm getting 1.2 mls per hour. Answered by Florencio Lovett 1 year ago.


Drugs for bradycardia with symptoms?
What drugs does a nurse give to a patient when they are in symptomtic bradycardia? Asked by Latricia Goffman 1 year ago.

In an emergency situation atropine,isuprel. Answered by Dan Hubner 1 year ago.

I'm not sure what your question really is, but if you have ANY questions about bradycardia or its symptoms, you can go to www.webmd.com and search under bradycardia, symptoms or bradycardia, medications. WebMD is an outstanding, authoritative, reliable medical website. Answered by India Syer 1 year ago.


Asthma results in the constriction of bronchioles. What chemical will reverse it?
Asked by Cinda Amory 1 year ago.

All brochodilalators are derivative of epinephrine. They started by trying to limit the Beat 1 agonists with Isuprel. Then further refinement led to Bronkosol, Alupent and now Albuterol sulfate. This is a Beta 2 agonists with very few side effects that were seen with earlier preparations. But these are all bronchodilators, a muscle relaxant for the bronchial airway muscles. That's not the only cause of constriction though. You have to consider the inflammation and consequent swelling of the bronchial walls. Also increased production of thick viscous mucous is a major contributing factor. Answered by Michiko Zeringue 1 year ago.

Medications can reverse the constriction caused by asthma that in turn causes inflamed airways. There are several medications used to treat asthma: -Bronchodliators: these medications contain a drug that opens the airways and come in short-acting or long-acting forms. Short acting bronchodliators such as salbutamol/albuterol [Ventolin] are taken when symptoms occur and begin working immediately and peak within 5-15 minutes to relieve symptoms. Short acting bronchodilators are also used by many asthmatics before exercise to prevent exercise induced asthma flares. In asthma treatment, except for in mild intermittent asthma, controller medications are usually needed, and are taken daily. This is where long acting bronchodilators can come into play: Long-acting bronchodilators are used in combination with corticosteroids [Advair is a combination inhaler, Serevent just contains a long acting bronchodilator]. These peak within 15-20 minutes, and their effects last for 12 hours to control asthma symptoms. These should not be used during an asthma flare, that's what the short-acting bronchodilator is for. -Corticosteroids come in either an inhaled, oral or injected form, but for maintenance therapy typically are used in the inhaled form through a puffer or 'diskus' device. Examples of inhaled corticosteroids are FloVent, QVar, Alvesco and Symbicort. These are typically inhaled twice a day, except for Alvesco, which has once-daily dosing. Oral corticosteroids [Prednisone] contain much higher doses and have much higher risk for side effects than inhaled corticosteroids. They are typically used in asthma emergencies or to head off a serious asthma attack that's already started. Injected corticosteroids are typically used when a patient is unresponsive, undergoing respiratory distress, in an emergency situation to bring down serious inflammation in the airways. -Leukotriene receptor antagonists aka leukotriene modifiers are taken in pill form and work differently than corticosteroids to reduce inflammation in the airways. Leukotriene receptor antagonists [Singulair] work to block leukotrienes released in the airways that cause inflammation, specifically in allergic asthma. Leukotriene modifiers can also be taken 2 hours prior to exercise to prevent exercise induced asthma. Either an inhaled corticosteroid or a leukotriene modifier is first-line asthma controller treatment. If a person is using their fast-acting bronchodilator [ventolin] more than 3 times a week except for before exercise, they should be on a controller medication. If adequate control isn't achieved after adding an inhaled corticosteroid, a leukotriene modifier may be added, or vice versa. Next up is the long-acting bronchodilator, then, if need be and typically only in severe cases, oral corticosteroids to get a flare under control. Answered by Keisha Pok 1 year ago.

asthma results constriction bronchioles chemical reverse Answered by Roxanne Armenteros 1 year ago.

The Chinese way of curing the asthma is to consume bird nest soup. For more detail please log on to www.qqbirdnest.com Answered by Estelle Hyter 1 year ago.

Albuterol a bronchodilater. atrovent sometimes. albuterol is the emergency bronchodilater. Answered by Cora Moudry 1 year ago.


Will sympathomimetic drug help a person with asthma?
Asked by Louisa Hertzog 1 year ago.

A sympathomimetic drug is the bronchodilators doctors prescribe for people with asthma or conditions with asthmatic components to it. These include, Isuprel, Bronkosol, Alupent, Albuterol etc. The body has two systems of autonomic nerves. Sympathetic and the parasympathetic. Where one does one thing the other does the opposite. The term sympathomimetic means something that will "mimic" the sympathetic nervous system. Sympathomimetics dilate or relax the bronchial muscles so you can see it would be very useful in asthmatic patients. As I said there are two systems so another approach some doctors use is to give the patient a parasympatholytic medicine (Atrovent) to reduce the influence of the parasympathetic system.They will give a sympathomimetic and a parasympatholytic at the same time. God bless. Answered by Kyle Marcellino 1 year ago.

idk, do BITCHES EAT 'SCREAM? (ice cream) listen, dont ask on yahoo answers. no one here has a medical degree, save 1 or 2 Answered by Louetta Sankowski 1 year ago.


Tilt Table Test (TTT)?
The hospital where I'm having it done uses the EP Lab and they do use Isuprel if necessary. That is the reason for my questions concerning arrhythmias. Asked by Martine Mittlestadt 1 year ago.

I am scheduled for a TTT next Tuesday and I have a few questions. I am a 5'3, 110 pound female. I have PVCs (trigeminy and bigeminy), PACS, mitral valve prolapse, sinus bradycardia, sinus tachycardia, and a sinus arrhythmia. My EP attempted to do a PVC ablation on Monday, but when he got in he found that they originate in the left ventricle and he said it would pose too many risks because of my "small frame." I get lightheaded and dizzy multiple times each day. These episodes are tied to the PVC runs--an extended run of trigeminy or bigeminy always precedes the incidents of lightheadedness and full syncope. There may be an opportunity for a second EPS and an ablation at a larger facility (Cleveland Clinic) who would be able to use a smaller balloon. Because my EP could not do the ablation, he ordered a TTT just to make sure there isn't any autonomic dysfunction as well. My questions are as follows: 1. Will my electrophysiologist or some another physician be in the room during the test in case something happens? 2. Will they stop the test early if too much arrhythmia is present, or will they only stop it prematurely if I actually faint? 3. If my EP is not present during the test, will he receive a a report of the arrhythmias that occurred during the test, or will he only get a list of my blood pressure and heart rate at various points? 4. Must a person actually faint for them to have a positive TTT, or do those administering the test evaluate other symptoms that occurred as well? Thank you so much. Answered by Eleanor Morgensen 1 year ago.

It is highly unlikely that a tilt table test will induce an irregular heart beat in you. All that is involved in a tilt table test is that a nurse checks your blood pressure and pulse with the table flat, then they elevate the head of the table and lower the foot of the table gradually, rechecking your blood pressure and pulse with the table at different angles. If your blood pressure drops too low or your heart rate rises too fast, then that is a positive TTT...there's no reason to push it further until you actually faint. Answered by Ronni Francis 1 year ago.

Vasovagal Syncope? Might be Carotid Sinus Syncope. Sounds love it might be triggered through Central Ischaemic reaction, that is the brains reaction to loss of blood to the mind. Maybe you've got a blockage? Answered by Elodia Scipioni 1 year ago.


PVCs - Where to go from here?
I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. ... Asked by Deanne Schmiel 1 year ago.

I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. They have lasted as long as eight hours. I finally made an appointment with an electrophysiologist in Toledo in October because the palpitations, lightheadedness, fatigue, and shortness of breath were getting unmanageable. I do not smoke, take recreational drugs, drink caffeine or alcohol, or anything of that nature. After the results of a 30-day event monitor came back in early December, my EP ordered a stress test and a Holter. Fortunately for me, but unfortunately for diagnostic purposes, I ended up having an unusually good day in terms of symptoms when I had the Holter and it only showed 10,000 PVCs. That is still a fair number. At my next appointment, when my EP reviewed the Holter and the stress test and I let him know that my symptoms were getting worse, he said “I really need to get in there to see what’s going on.” He also said that he thought he could “find at least a few spots to ablate.” I asked him if he could tell which side the PVCs were coming from and he said he thought the left. Because I was hesitant to consent to the EPS and ablation at that point, he put me on 12.5 mg Toprol. I had to go off of it within three days because I could not tolerate it. I came to my next appointment with a list of questions about the ablation and I was prepared to consent. My EP walks into the room and says “I will only do it if you can’t live with the PVCs.” There were no other intervening tests that could account for his change in tone. Anyway, after going back and forth a few times I finally had the EPS on Monday, March 7. For whatever reason, there were no PVCs at baseline, so he had to induce them with Isuprel. He came out of the control center and told me that they were coming from the left side and that he was not going to do the ablation because it was pose “too much of a risk to inflate the balloon in someone with such a small frame.” He also let me know that they were “severely limited in what we can do because of your past paradoxical reaction to Versed.” He used Demerol instead which immediately suppressed the PVCs for the rest of the study. There may have been a few, but the Demerol definitely toned them down. Even after he decided not to do the ablation, he put one catheter in my right femoral vein and did the pacing and some other things. QUESTIONS: --I am the same size now as I was in December. As I related above, at that time my EP thought he could find at least a few spots to ablate and he thought they would be in the left ventricle. On Monday, he would not do the ablation because of the dangers inherent in left ventricle ablations in someone with a “small frame.” He is inconsistent and inconsistent about important things. It honestly seems like a situation where my case is too complex for him and their facility, but he does not want to admit it. My friends, many of who are in the medical field are encouraging me to seek a second opinion if not switch doctors completely. Based on the evidence, would you recommend this as well? I am only about two hours from the Cleveland Clinic and I know that they do pediatric ablations, so they would have a smaller balloon if that is needed. --I had a paradoxical reaction to Versed 11 years ago. On Monday, they used 75mg of Demerol and that immediately stopped the PVCs. Is it possible for a person to have a paradoxical reaction to a drug and then have them react normally to it years later? My EP made a huge deal of how important it was to use Versed. --My EP is now suddenly blaming all of my symptoms on the mitral valve prolapse. He said the MVP was “mild.” I may be missing something, but that does not make sense. Am I missing something? --My EP scheduled me for a TTT on Tuesday. Is there a doctor present for the test? I know they sometimes use Isuprel to increase the heart rate, and that would induce a long run of PVCs in me and possible fainting if I am tilted up on the table. I realize that the purpose of the test is to induce syncope, but because the arrhythmia is so frequent with me and I do have attendant symptoms it might be good if a medical professional were in the room just in case! Thank you Jenn Answered by Leanne Trudgeon 1 year ago.

Except for the unpleasant symptoms that they cause, PVCs like you have are benign--if you were not aware of them (and many people have 10s of thousands of PVCs/day and don't know it), they could be completely ignored. But since yours are on the left side, there would be some risk in attempting an ablation, as clots can always form during that procedure, and the left ventricle sends its blood directly to the brain. Hence you would be risking a stroke to treat a benign condition. If that were to happen, your cardiologist would be subject to justifiable criticism for doing the procedure. That may be part of this reason for his hesitancy. Some comments: >I am assuming that your echocardiogram has shown normal heart function. >There is absolutely no evidence that MVP causes PVCs, and the old concept of "MVP syndrome" has been discredited for years. Its only importance is if it causes mitral regurgitation, which does not appear to be the case with you. >I am not an EP specialist, but my understanding of ablation is that it involves either freezing or burning (with a radio frequency current) the tissue that is generating the PVCs. It does not involve a balloon for the kind of procedure that you would need. (It can involve piercing a small hole in the septum between the right and left atria; possibly that could raise a concern in someone with a "small frame.") >I do not understand the reason for the TTT. It makes no sense to me, but then all I know about your case is your brief summary... >If Toprol is the only try at medical management that you've had, you should investigate other drugs. But in any case, it appears that you and your cardiologist are not a good match. Find someone else. Answered by Sonny Boutet 1 year ago.

conventional untimely ventricular contractions. %. originate whilst another part of the middle (in the ventricles) than it relatively is organic heartbeat inititator initiates a beat. Answered by Lyndsay Eschmann 1 year ago.


Why does the bronchodilator exaggerate the tachycardia?
Asked by Shakita Yong 1 year ago.

Bronchodilators were originally alpha or beta agonists. The grandfather of all of them is epinephrine.(Norepinephrine was primarily an alpha agonist and used mostly to treat kids with Croup.) Both of which would relax the bronchial muscles but had the side effect of increasing the heart rate. Through research it was found the the beta receptors were of two types, Beta 1 and beta 2. Beta 1 increased the heart rate while beta 2 relaxed the bronchial muscles. The pharmaceutical companies further refined the epinephrine to stimulate only the beta 2 receptors. They also refined it to block the beta 1 effects becoming the class of drugs known as beta blockers.This was used in tachyarrythmnias. Isuprel was the first beta agonist and it was very effective and fast acting but there was still a lot of beta 1 activity. Then came Bronkosol(Isoetharine) which seemed to have solved the problem. Alupent was next. Finally Albuterol was introduced which had virtually no beta 1 activity. The onset of activity was longer(up to 5 min.) but the effect on heart rate was much less. Some people still get an increase in heart rate with Albuterol but the percentage is very small. You still have to monitor the patient for heart rate increase but the likelihood is much less. I should have explained at the beginning that there are two types of nerves in the peripheral nervous system. Sympathetic and parasympathetic. While one has one effect the other has the opposite effect. Epinepherine is a sympathomimetic or "mimics" the sympathetic nerves. A drug which stimulates the parasympathetic system would be a parasympathomimetic. Any drug that reduces the effect of one of these is said to "lyse" the effect. So a drug which reduced the parasympathetic system would be called a parasympatholytic. The sympathetic system dilates or relaxes the bronchial muscles and the parasympathetic system constricts them. If you were to give a sympathomimetic and a parasympatholytic at the same time you would be attacking the problem from two sides. Atrovent is a parasympatholytic drug often given with Albuterol and is called Combivent. Studies have shown that in certain patients the bronchodilator effect is enhanced by the addition of Atrovent. God bless. Answered by Kimbra Batcher 1 year ago.

because it has beta 1 receptor effect at the heart...which when stimulated caused an increased in heart beat Answered by Samual Goeldner 1 year ago.


Why should one use a bronchodilator before a corticosteroid?
A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first,... Asked by Corene Hosey 1 year ago.

A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first, then the steroid inhaler. -Rekha, RN/BSN Answered by Stan Lulow 1 year ago.

Bronchodilators work systemically. They have no local effect. It's absorbed into the mucosa and thereby the blood vessels. Don't forget it has to be absorbed through the mucous layer and then the inflamed mucosa before it gets anywhere near the bronchial musculature. And, being Beta 2 agonists they only relax the bronchial muscles. They do not relieve inflammation. The saline is a mucolytic and works faster and locally. Of course, this is when you are taking the unit dose. If you are using the metered dose inhaler (MDI) there is no saline so it's best to wait 5 minutes for the full effect before taking the steroid. Once you cough the mucous out the bronchodilator can get to the membrane and be absorbed into the circulation faster. It is doing no good being absorbed by the mucous itself. Albuterol is the chemical evolutionary end product of epinephrine for the relief of bronchospasm. Epinephrine, of course, has primarily beta 1 and beta 2 effects. and it's very fast acting but it only lasts for maybe an hour. Isuprel was the next step. It's onset of effect was about 2 minutes but it remained effective for about two hours and the dose, as with epinephrine, had to be titred to the patient's heart rate. Bronkosol was the next in line. It's peak effect was achieved in 3-4 minutes but only lasted 3 hours. Alupent was about the same. Albuterol achieves it's maximum effect in 5 minutes and lasts for about 4 hours. All these meds were created in an attempt to mitigate the cardiac side effects by making them less beta 1 and more beta 2 agonists. Norepinephrine is primarily an alpha agonist and used, in titred doses, for acute laryngotracheobronchitis in children providing a fast acting anti inflammatory. Now once the bronchodilator is absorbed you can get maximum penetration of the steroid for it's localized effect on the inflammation and swelling. Also, a good tip is, if you are ordered to take two puffs from the MDI, wait 5 minutes between puffs so you get maximum effect from the first puff and the second one will get deeper. I know it's hard to wait but I always told my patients this and they all remarked what a difference it makes. Answered by Gavin Huirgs 1 year ago.

Because if you relax and open the airways first, then the steriod can better penetrate the lungs to reduce inflammation. Answered by Jann Anzalone 1 year ago.

ASKED AND ANSWERED. THANKS FOR THE POINTS! Answered by Kyle Drenner 1 year ago.


Ml/hr (dosage/wt or BSA/hr or min prescribed)?
Isuprel is to be infused at a rate of 0.05mcg/kg/minute. 1mg of Isuprel has been added to destrose 5% water. The final solution has a total volume of 50ml. Your patients current weight is 22lbs. The IV should be infused at how many ml per hr? Asked by Tabatha Graven 1 year ago.

1000 mcgs in 50 mls, turns out to be 30mcg per hour..i'm getting 1.2 mls per hour. Answered by Whitney Decastro 1 year ago.


Drugs for bradycardia with symptoms?
What drugs does a nurse give to a patient when they are in symptomtic bradycardia? Asked by Gerry Wilhelmi 1 year ago.

In an emergency situation atropine,isuprel. Answered by Renea Myricks 1 year ago.

I'm not sure what your question really is, but if you have ANY questions about bradycardia or its symptoms, you can go to www.webmd.com and search under bradycardia, symptoms or bradycardia, medications. WebMD is an outstanding, authoritative, reliable medical website. Answered by Penni Demott 1 year ago.


Asthma results in the constriction of bronchioles. What chemical will reverse it?
Asked by Jerome Neaves 1 year ago.

All brochodilalators are derivative of epinephrine. They started by trying to limit the Beat 1 agonists with Isuprel. Then further refinement led to Bronkosol, Alupent and now Albuterol sulfate. This is a Beta 2 agonists with very few side effects that were seen with earlier preparations. But these are all bronchodilators, a muscle relaxant for the bronchial airway muscles. That's not the only cause of constriction though. You have to consider the inflammation and consequent swelling of the bronchial walls. Also increased production of thick viscous mucous is a major contributing factor. Answered by Eboni Cowels 1 year ago.

Medications can reverse the constriction caused by asthma that in turn causes inflamed airways. There are several medications used to treat asthma: -Bronchodliators: these medications contain a drug that opens the airways and come in short-acting or long-acting forms. Short acting bronchodliators such as salbutamol/albuterol [Ventolin] are taken when symptoms occur and begin working immediately and peak within 5-15 minutes to relieve symptoms. Short acting bronchodilators are also used by many asthmatics before exercise to prevent exercise induced asthma flares. In asthma treatment, except for in mild intermittent asthma, controller medications are usually needed, and are taken daily. This is where long acting bronchodilators can come into play: Long-acting bronchodilators are used in combination with corticosteroids [Advair is a combination inhaler, Serevent just contains a long acting bronchodilator]. These peak within 15-20 minutes, and their effects last for 12 hours to control asthma symptoms. These should not be used during an asthma flare, that's what the short-acting bronchodilator is for. -Corticosteroids come in either an inhaled, oral or injected form, but for maintenance therapy typically are used in the inhaled form through a puffer or 'diskus' device. Examples of inhaled corticosteroids are FloVent, QVar, Alvesco and Symbicort. These are typically inhaled twice a day, except for Alvesco, which has once-daily dosing. Oral corticosteroids [Prednisone] contain much higher doses and have much higher risk for side effects than inhaled corticosteroids. They are typically used in asthma emergencies or to head off a serious asthma attack that's already started. Injected corticosteroids are typically used when a patient is unresponsive, undergoing respiratory distress, in an emergency situation to bring down serious inflammation in the airways. -Leukotriene receptor antagonists aka leukotriene modifiers are taken in pill form and work differently than corticosteroids to reduce inflammation in the airways. Leukotriene receptor antagonists [Singulair] work to block leukotrienes released in the airways that cause inflammation, specifically in allergic asthma. Leukotriene modifiers can also be taken 2 hours prior to exercise to prevent exercise induced asthma. Either an inhaled corticosteroid or a leukotriene modifier is first-line asthma controller treatment. If a person is using their fast-acting bronchodilator [ventolin] more than 3 times a week except for before exercise, they should be on a controller medication. If adequate control isn't achieved after adding an inhaled corticosteroid, a leukotriene modifier may be added, or vice versa. Next up is the long-acting bronchodilator, then, if need be and typically only in severe cases, oral corticosteroids to get a flare under control. Answered by Apolonia Dolfi 1 year ago.

asthma results constriction bronchioles chemical reverse Answered by Parker Degruy 1 year ago.

The Chinese way of curing the asthma is to consume bird nest soup. For more detail please log on to www.qqbirdnest.com Answered by Albertine Brailsford 1 year ago.

Albuterol a bronchodilater. atrovent sometimes. albuterol is the emergency bronchodilater. Answered by Joellen Tang 1 year ago.


Will sympathomimetic drug help a person with asthma?
Asked by Venetta Fahrenkrug 1 year ago.

A sympathomimetic drug is the bronchodilators doctors prescribe for people with asthma or conditions with asthmatic components to it. These include, Isuprel, Bronkosol, Alupent, Albuterol etc. The body has two systems of autonomic nerves. Sympathetic and the parasympathetic. Where one does one thing the other does the opposite. The term sympathomimetic means something that will "mimic" the sympathetic nervous system. Sympathomimetics dilate or relax the bronchial muscles so you can see it would be very useful in asthmatic patients. As I said there are two systems so another approach some doctors use is to give the patient a parasympatholytic medicine (Atrovent) to reduce the influence of the parasympathetic system.They will give a sympathomimetic and a parasympatholytic at the same time. God bless. Answered by Omega Yeaman 1 year ago.

idk, do BITCHES EAT 'SCREAM? (ice cream) listen, dont ask on yahoo answers. no one here has a medical degree, save 1 or 2 Answered by Keneth Gahring 1 year ago.


Tilt Table Test (TTT)?
The hospital where I'm having it done uses the EP Lab and they do use Isuprel if necessary. That is the reason for my questions concerning arrhythmias. Asked by Ricardo Warchal 1 year ago.

I am scheduled for a TTT next Tuesday and I have a few questions. I am a 5'3, 110 pound female. I have PVCs (trigeminy and bigeminy), PACS, mitral valve prolapse, sinus bradycardia, sinus tachycardia, and a sinus arrhythmia. My EP attempted to do a PVC ablation on Monday, but when he got in he found that they originate in the left ventricle and he said it would pose too many risks because of my "small frame." I get lightheaded and dizzy multiple times each day. These episodes are tied to the PVC runs--an extended run of trigeminy or bigeminy always precedes the incidents of lightheadedness and full syncope. There may be an opportunity for a second EPS and an ablation at a larger facility (Cleveland Clinic) who would be able to use a smaller balloon. Because my EP could not do the ablation, he ordered a TTT just to make sure there isn't any autonomic dysfunction as well. My questions are as follows: 1. Will my electrophysiologist or some another physician be in the room during the test in case something happens? 2. Will they stop the test early if too much arrhythmia is present, or will they only stop it prematurely if I actually faint? 3. If my EP is not present during the test, will he receive a a report of the arrhythmias that occurred during the test, or will he only get a list of my blood pressure and heart rate at various points? 4. Must a person actually faint for them to have a positive TTT, or do those administering the test evaluate other symptoms that occurred as well? Thank you so much. Answered by Kellie Terazes 1 year ago.

It is highly unlikely that a tilt table test will induce an irregular heart beat in you. All that is involved in a tilt table test is that a nurse checks your blood pressure and pulse with the table flat, then they elevate the head of the table and lower the foot of the table gradually, rechecking your blood pressure and pulse with the table at different angles. If your blood pressure drops too low or your heart rate rises too fast, then that is a positive TTT...there's no reason to push it further until you actually faint. Answered by Mora Champagne 1 year ago.

Vasovagal Syncope? Might be Carotid Sinus Syncope. Sounds love it might be triggered through Central Ischaemic reaction, that is the brains reaction to loss of blood to the mind. Maybe you've got a blockage? Answered by Valentine Decasas 1 year ago.


PVCs - Where to go from here?
I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. ... Asked by Karoline Mendez 1 year ago.

I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. They have lasted as long as eight hours. I finally made an appointment with an electrophysiologist in Toledo in October because the palpitations, lightheadedness, fatigue, and shortness of breath were getting unmanageable. I do not smoke, take recreational drugs, drink caffeine or alcohol, or anything of that nature. After the results of a 30-day event monitor came back in early December, my EP ordered a stress test and a Holter. Fortunately for me, but unfortunately for diagnostic purposes, I ended up having an unusually good day in terms of symptoms when I had the Holter and it only showed 10,000 PVCs. That is still a fair number. At my next appointment, when my EP reviewed the Holter and the stress test and I let him know that my symptoms were getting worse, he said “I really need to get in there to see what’s going on.” He also said that he thought he could “find at least a few spots to ablate.” I asked him if he could tell which side the PVCs were coming from and he said he thought the left. Because I was hesitant to consent to the EPS and ablation at that point, he put me on 12.5 mg Toprol. I had to go off of it within three days because I could not tolerate it. I came to my next appointment with a list of questions about the ablation and I was prepared to consent. My EP walks into the room and says “I will only do it if you can’t live with the PVCs.” There were no other intervening tests that could account for his change in tone. Anyway, after going back and forth a few times I finally had the EPS on Monday, March 7. For whatever reason, there were no PVCs at baseline, so he had to induce them with Isuprel. He came out of the control center and told me that they were coming from the left side and that he was not going to do the ablation because it was pose “too much of a risk to inflate the balloon in someone with such a small frame.” He also let me know that they were “severely limited in what we can do because of your past paradoxical reaction to Versed.” He used Demerol instead which immediately suppressed the PVCs for the rest of the study. There may have been a few, but the Demerol definitely toned them down. Even after he decided not to do the ablation, he put one catheter in my right femoral vein and did the pacing and some other things. QUESTIONS: --I am the same size now as I was in December. As I related above, at that time my EP thought he could find at least a few spots to ablate and he thought they would be in the left ventricle. On Monday, he would not do the ablation because of the dangers inherent in left ventricle ablations in someone with a “small frame.” He is inconsistent and inconsistent about important things. It honestly seems like a situation where my case is too complex for him and their facility, but he does not want to admit it. My friends, many of who are in the medical field are encouraging me to seek a second opinion if not switch doctors completely. Based on the evidence, would you recommend this as well? I am only about two hours from the Cleveland Clinic and I know that they do pediatric ablations, so they would have a smaller balloon if that is needed. --I had a paradoxical reaction to Versed 11 years ago. On Monday, they used 75mg of Demerol and that immediately stopped the PVCs. Is it possible for a person to have a paradoxical reaction to a drug and then have them react normally to it years later? My EP made a huge deal of how important it was to use Versed. --My EP is now suddenly blaming all of my symptoms on the mitral valve prolapse. He said the MVP was “mild.” I may be missing something, but that does not make sense. Am I missing something? --My EP scheduled me for a TTT on Tuesday. Is there a doctor present for the test? I know they sometimes use Isuprel to increase the heart rate, and that would induce a long run of PVCs in me and possible fainting if I am tilted up on the table. I realize that the purpose of the test is to induce syncope, but because the arrhythmia is so frequent with me and I do have attendant symptoms it might be good if a medical professional were in the room just in case! Thank you Jenn Answered by Scottie Wice 1 year ago.

Except for the unpleasant symptoms that they cause, PVCs like you have are benign--if you were not aware of them (and many people have 10s of thousands of PVCs/day and don't know it), they could be completely ignored. But since yours are on the left side, there would be some risk in attempting an ablation, as clots can always form during that procedure, and the left ventricle sends its blood directly to the brain. Hence you would be risking a stroke to treat a benign condition. If that were to happen, your cardiologist would be subject to justifiable criticism for doing the procedure. That may be part of this reason for his hesitancy. Some comments: >I am assuming that your echocardiogram has shown normal heart function. >There is absolutely no evidence that MVP causes PVCs, and the old concept of "MVP syndrome" has been discredited for years. Its only importance is if it causes mitral regurgitation, which does not appear to be the case with you. >I am not an EP specialist, but my understanding of ablation is that it involves either freezing or burning (with a radio frequency current) the tissue that is generating the PVCs. It does not involve a balloon for the kind of procedure that you would need. (It can involve piercing a small hole in the septum between the right and left atria; possibly that could raise a concern in someone with a "small frame.") >I do not understand the reason for the TTT. It makes no sense to me, but then all I know about your case is your brief summary... >If Toprol is the only try at medical management that you've had, you should investigate other drugs. But in any case, it appears that you and your cardiologist are not a good match. Find someone else. Answered by Deidre Hyett 1 year ago.

conventional untimely ventricular contractions. %. originate whilst another part of the middle (in the ventricles) than it relatively is organic heartbeat inititator initiates a beat. Answered by Domonique Stirna 1 year ago.


Why does the bronchodilator exaggerate the tachycardia?
Asked by Orlando Youket 1 year ago.

Bronchodilators were originally alpha or beta agonists. The grandfather of all of them is epinephrine.(Norepinephrine was primarily an alpha agonist and used mostly to treat kids with Croup.) Both of which would relax the bronchial muscles but had the side effect of increasing the heart rate. Through research it was found the the beta receptors were of two types, Beta 1 and beta 2. Beta 1 increased the heart rate while beta 2 relaxed the bronchial muscles. The pharmaceutical companies further refined the epinephrine to stimulate only the beta 2 receptors. They also refined it to block the beta 1 effects becoming the class of drugs known as beta blockers.This was used in tachyarrythmnias. Isuprel was the first beta agonist and it was very effective and fast acting but there was still a lot of beta 1 activity. Then came Bronkosol(Isoetharine) which seemed to have solved the problem. Alupent was next. Finally Albuterol was introduced which had virtually no beta 1 activity. The onset of activity was longer(up to 5 min.) but the effect on heart rate was much less. Some people still get an increase in heart rate with Albuterol but the percentage is very small. You still have to monitor the patient for heart rate increase but the likelihood is much less. I should have explained at the beginning that there are two types of nerves in the peripheral nervous system. Sympathetic and parasympathetic. While one has one effect the other has the opposite effect. Epinepherine is a sympathomimetic or "mimics" the sympathetic nerves. A drug which stimulates the parasympathetic system would be a parasympathomimetic. Any drug that reduces the effect of one of these is said to "lyse" the effect. So a drug which reduced the parasympathetic system would be called a parasympatholytic. The sympathetic system dilates or relaxes the bronchial muscles and the parasympathetic system constricts them. If you were to give a sympathomimetic and a parasympatholytic at the same time you would be attacking the problem from two sides. Atrovent is a parasympatholytic drug often given with Albuterol and is called Combivent. Studies have shown that in certain patients the bronchodilator effect is enhanced by the addition of Atrovent. God bless. Answered by Chieko Ebling 1 year ago.

because it has beta 1 receptor effect at the heart...which when stimulated caused an increased in heart beat Answered by Fredia Darkis 1 year ago.


Why should one use a bronchodilator before a corticosteroid?
A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first,... Asked by Carmelia Kobryn 1 year ago.

A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first, then the steroid inhaler. -Rekha, RN/BSN Answered by Ginny Shiyou 1 year ago.

Bronchodilators work systemically. They have no local effect. It's absorbed into the mucosa and thereby the blood vessels. Don't forget it has to be absorbed through the mucous layer and then the inflamed mucosa before it gets anywhere near the bronchial musculature. And, being Beta 2 agonists they only relax the bronchial muscles. They do not relieve inflammation. The saline is a mucolytic and works faster and locally. Of course, this is when you are taking the unit dose. If you are using the metered dose inhaler (MDI) there is no saline so it's best to wait 5 minutes for the full effect before taking the steroid. Once you cough the mucous out the bronchodilator can get to the membrane and be absorbed into the circulation faster. It is doing no good being absorbed by the mucous itself. Albuterol is the chemical evolutionary end product of epinephrine for the relief of bronchospasm. Epinephrine, of course, has primarily beta 1 and beta 2 effects. and it's very fast acting but it only lasts for maybe an hour. Isuprel was the next step. It's onset of effect was about 2 minutes but it remained effective for about two hours and the dose, as with epinephrine, had to be titred to the patient's heart rate. Bronkosol was the next in line. It's peak effect was achieved in 3-4 minutes but only lasted 3 hours. Alupent was about the same. Albuterol achieves it's maximum effect in 5 minutes and lasts for about 4 hours. All these meds were created in an attempt to mitigate the cardiac side effects by making them less beta 1 and more beta 2 agonists. Norepinephrine is primarily an alpha agonist and used, in titred doses, for acute laryngotracheobronchitis in children providing a fast acting anti inflammatory. Now once the bronchodilator is absorbed you can get maximum penetration of the steroid for it's localized effect on the inflammation and swelling. Also, a good tip is, if you are ordered to take two puffs from the MDI, wait 5 minutes between puffs so you get maximum effect from the first puff and the second one will get deeper. I know it's hard to wait but I always told my patients this and they all remarked what a difference it makes. Answered by Audrie Baldelli 1 year ago.

Because if you relax and open the airways first, then the steriod can better penetrate the lungs to reduce inflammation. Answered by Melvina Finken 1 year ago.

ASKED AND ANSWERED. THANKS FOR THE POINTS! Answered by Tena Salmela 1 year ago.


Ml/hr (dosage/wt or BSA/hr or min prescribed)?
Isuprel is to be infused at a rate of 0.05mcg/kg/minute. 1mg of Isuprel has been added to destrose 5% water. The final solution has a total volume of 50ml. Your patients current weight is 22lbs. The IV should be infused at how many ml per hr? Asked by Porsha Saballos 1 year ago.

1000 mcgs in 50 mls, turns out to be 30mcg per hour..i'm getting 1.2 mls per hour. Answered by Kristan Keets 1 year ago.


Drugs for bradycardia with symptoms?
What drugs does a nurse give to a patient when they are in symptomtic bradycardia? Asked by Bertram Frodsham 1 year ago.

In an emergency situation atropine,isuprel. Answered by Paris Tarrance 1 year ago.

I'm not sure what your question really is, but if you have ANY questions about bradycardia or its symptoms, you can go to www.webmd.com and search under bradycardia, symptoms or bradycardia, medications. WebMD is an outstanding, authoritative, reliable medical website. Answered by Catrina Stoutamire 1 year ago.


Asthma results in the constriction of bronchioles. What chemical will reverse it?
Asked by Felecia Rohrbaugh 1 year ago.

All brochodilalators are derivative of epinephrine. They started by trying to limit the Beat 1 agonists with Isuprel. Then further refinement led to Bronkosol, Alupent and now Albuterol sulfate. This is a Beta 2 agonists with very few side effects that were seen with earlier preparations. But these are all bronchodilators, a muscle relaxant for the bronchial airway muscles. That's not the only cause of constriction though. You have to consider the inflammation and consequent swelling of the bronchial walls. Also increased production of thick viscous mucous is a major contributing factor. Answered by Joey Bangert 1 year ago.

Medications can reverse the constriction caused by asthma that in turn causes inflamed airways. There are several medications used to treat asthma: -Bronchodliators: these medications contain a drug that opens the airways and come in short-acting or long-acting forms. Short acting bronchodliators such as salbutamol/albuterol [Ventolin] are taken when symptoms occur and begin working immediately and peak within 5-15 minutes to relieve symptoms. Short acting bronchodilators are also used by many asthmatics before exercise to prevent exercise induced asthma flares. In asthma treatment, except for in mild intermittent asthma, controller medications are usually needed, and are taken daily. This is where long acting bronchodilators can come into play: Long-acting bronchodilators are used in combination with corticosteroids [Advair is a combination inhaler, Serevent just contains a long acting bronchodilator]. These peak within 15-20 minutes, and their effects last for 12 hours to control asthma symptoms. These should not be used during an asthma flare, that's what the short-acting bronchodilator is for. -Corticosteroids come in either an inhaled, oral or injected form, but for maintenance therapy typically are used in the inhaled form through a puffer or 'diskus' device. Examples of inhaled corticosteroids are FloVent, QVar, Alvesco and Symbicort. These are typically inhaled twice a day, except for Alvesco, which has once-daily dosing. Oral corticosteroids [Prednisone] contain much higher doses and have much higher risk for side effects than inhaled corticosteroids. They are typically used in asthma emergencies or to head off a serious asthma attack that's already started. Injected corticosteroids are typically used when a patient is unresponsive, undergoing respiratory distress, in an emergency situation to bring down serious inflammation in the airways. -Leukotriene receptor antagonists aka leukotriene modifiers are taken in pill form and work differently than corticosteroids to reduce inflammation in the airways. Leukotriene receptor antagonists [Singulair] work to block leukotrienes released in the airways that cause inflammation, specifically in allergic asthma. Leukotriene modifiers can also be taken 2 hours prior to exercise to prevent exercise induced asthma. Either an inhaled corticosteroid or a leukotriene modifier is first-line asthma controller treatment. If a person is using their fast-acting bronchodilator [ventolin] more than 3 times a week except for before exercise, they should be on a controller medication. If adequate control isn't achieved after adding an inhaled corticosteroid, a leukotriene modifier may be added, or vice versa. Next up is the long-acting bronchodilator, then, if need be and typically only in severe cases, oral corticosteroids to get a flare under control. Answered by Rayford Mcquigg 1 year ago.

asthma results constriction bronchioles chemical reverse Answered by Reyna Brilla 1 year ago.

The Chinese way of curing the asthma is to consume bird nest soup. For more detail please log on to www.qqbirdnest.com Answered by Veda Stuekerjuerge 1 year ago.

Albuterol a bronchodilater. atrovent sometimes. albuterol is the emergency bronchodilater. Answered by Houston Molinini 1 year ago.


Will sympathomimetic drug help a person with asthma?
Asked by Addie Defeo 1 year ago.

A sympathomimetic drug is the bronchodilators doctors prescribe for people with asthma or conditions with asthmatic components to it. These include, Isuprel, Bronkosol, Alupent, Albuterol etc. The body has two systems of autonomic nerves. Sympathetic and the parasympathetic. Where one does one thing the other does the opposite. The term sympathomimetic means something that will "mimic" the sympathetic nervous system. Sympathomimetics dilate or relax the bronchial muscles so you can see it would be very useful in asthmatic patients. As I said there are two systems so another approach some doctors use is to give the patient a parasympatholytic medicine (Atrovent) to reduce the influence of the parasympathetic system.They will give a sympathomimetic and a parasympatholytic at the same time. God bless. Answered by Valorie Spevacek 1 year ago.

idk, do BITCHES EAT 'SCREAM? (ice cream) listen, dont ask on yahoo answers. no one here has a medical degree, save 1 or 2 Answered by Maxwell Mattina 1 year ago.


Tilt Table Test (TTT)?
The hospital where I'm having it done uses the EP Lab and they do use Isuprel if necessary. That is the reason for my questions concerning arrhythmias. Asked by Deirdre Glesener 1 year ago.

I am scheduled for a TTT next Tuesday and I have a few questions. I am a 5'3, 110 pound female. I have PVCs (trigeminy and bigeminy), PACS, mitral valve prolapse, sinus bradycardia, sinus tachycardia, and a sinus arrhythmia. My EP attempted to do a PVC ablation on Monday, but when he got in he found that they originate in the left ventricle and he said it would pose too many risks because of my "small frame." I get lightheaded and dizzy multiple times each day. These episodes are tied to the PVC runs--an extended run of trigeminy or bigeminy always precedes the incidents of lightheadedness and full syncope. There may be an opportunity for a second EPS and an ablation at a larger facility (Cleveland Clinic) who would be able to use a smaller balloon. Because my EP could not do the ablation, he ordered a TTT just to make sure there isn't any autonomic dysfunction as well. My questions are as follows: 1. Will my electrophysiologist or some another physician be in the room during the test in case something happens? 2. Will they stop the test early if too much arrhythmia is present, or will they only stop it prematurely if I actually faint? 3. If my EP is not present during the test, will he receive a a report of the arrhythmias that occurred during the test, or will he only get a list of my blood pressure and heart rate at various points? 4. Must a person actually faint for them to have a positive TTT, or do those administering the test evaluate other symptoms that occurred as well? Thank you so much. Answered by Elisabeth Gergel 1 year ago.

It is highly unlikely that a tilt table test will induce an irregular heart beat in you. All that is involved in a tilt table test is that a nurse checks your blood pressure and pulse with the table flat, then they elevate the head of the table and lower the foot of the table gradually, rechecking your blood pressure and pulse with the table at different angles. If your blood pressure drops too low or your heart rate rises too fast, then that is a positive TTT...there's no reason to push it further until you actually faint. Answered by Veronica Sanke 1 year ago.

Vasovagal Syncope? Might be Carotid Sinus Syncope. Sounds love it might be triggered through Central Ischaemic reaction, that is the brains reaction to loss of blood to the mind. Maybe you've got a blockage? Answered by Stefani Maguire 1 year ago.


PVCs - Where to go from here?
I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. ... Asked by Gillian Vignarath 1 year ago.

I am a 32-year-old 5’3, 110 pound female. My diagnoses are: PVCs (left ventricle), mild mitral valve prolapse, PACs, sinus arrhythmia, sinus bradycardia, sinus tachycardia, asthma, and scoliosis (spinal fusion 2/11/1988). I have had daily runs of ventricular trigeminy and ventricular bigeminy since July 2010. They have lasted as long as eight hours. I finally made an appointment with an electrophysiologist in Toledo in October because the palpitations, lightheadedness, fatigue, and shortness of breath were getting unmanageable. I do not smoke, take recreational drugs, drink caffeine or alcohol, or anything of that nature. After the results of a 30-day event monitor came back in early December, my EP ordered a stress test and a Holter. Fortunately for me, but unfortunately for diagnostic purposes, I ended up having an unusually good day in terms of symptoms when I had the Holter and it only showed 10,000 PVCs. That is still a fair number. At my next appointment, when my EP reviewed the Holter and the stress test and I let him know that my symptoms were getting worse, he said “I really need to get in there to see what’s going on.” He also said that he thought he could “find at least a few spots to ablate.” I asked him if he could tell which side the PVCs were coming from and he said he thought the left. Because I was hesitant to consent to the EPS and ablation at that point, he put me on 12.5 mg Toprol. I had to go off of it within three days because I could not tolerate it. I came to my next appointment with a list of questions about the ablation and I was prepared to consent. My EP walks into the room and says “I will only do it if you can’t live with the PVCs.” There were no other intervening tests that could account for his change in tone. Anyway, after going back and forth a few times I finally had the EPS on Monday, March 7. For whatever reason, there were no PVCs at baseline, so he had to induce them with Isuprel. He came out of the control center and told me that they were coming from the left side and that he was not going to do the ablation because it was pose “too much of a risk to inflate the balloon in someone with such a small frame.” He also let me know that they were “severely limited in what we can do because of your past paradoxical reaction to Versed.” He used Demerol instead which immediately suppressed the PVCs for the rest of the study. There may have been a few, but the Demerol definitely toned them down. Even after he decided not to do the ablation, he put one catheter in my right femoral vein and did the pacing and some other things. QUESTIONS: --I am the same size now as I was in December. As I related above, at that time my EP thought he could find at least a few spots to ablate and he thought they would be in the left ventricle. On Monday, he would not do the ablation because of the dangers inherent in left ventricle ablations in someone with a “small frame.” He is inconsistent and inconsistent about important things. It honestly seems like a situation where my case is too complex for him and their facility, but he does not want to admit it. My friends, many of who are in the medical field are encouraging me to seek a second opinion if not switch doctors completely. Based on the evidence, would you recommend this as well? I am only about two hours from the Cleveland Clinic and I know that they do pediatric ablations, so they would have a smaller balloon if that is needed. --I had a paradoxical reaction to Versed 11 years ago. On Monday, they used 75mg of Demerol and that immediately stopped the PVCs. Is it possible for a person to have a paradoxical reaction to a drug and then have them react normally to it years later? My EP made a huge deal of how important it was to use Versed. --My EP is now suddenly blaming all of my symptoms on the mitral valve prolapse. He said the MVP was “mild.” I may be missing something, but that does not make sense. Am I missing something? --My EP scheduled me for a TTT on Tuesday. Is there a doctor present for the test? I know they sometimes use Isuprel to increase the heart rate, and that would induce a long run of PVCs in me and possible fainting if I am tilted up on the table. I realize that the purpose of the test is to induce syncope, but because the arrhythmia is so frequent with me and I do have attendant symptoms it might be good if a medical professional were in the room just in case! Thank you Jenn Answered by Alexa Fijal 1 year ago.

Except for the unpleasant symptoms that they cause, PVCs like you have are benign--if you were not aware of them (and many people have 10s of thousands of PVCs/day and don't know it), they could be completely ignored. But since yours are on the left side, there would be some risk in attempting an ablation, as clots can always form during that procedure, and the left ventricle sends its blood directly to the brain. Hence you would be risking a stroke to treat a benign condition. If that were to happen, your cardiologist would be subject to justifiable criticism for doing the procedure. That may be part of this reason for his hesitancy. Some comments: >I am assuming that your echocardiogram has shown normal heart function. >There is absolutely no evidence that MVP causes PVCs, and the old concept of "MVP syndrome" has been discredited for years. Its only importance is if it causes mitral regurgitation, which does not appear to be the case with you. >I am not an EP specialist, but my understanding of ablation is that it involves either freezing or burning (with a radio frequency current) the tissue that is generating the PVCs. It does not involve a balloon for the kind of procedure that you would need. (It can involve piercing a small hole in the septum between the right and left atria; possibly that could raise a concern in someone with a "small frame.") >I do not understand the reason for the TTT. It makes no sense to me, but then all I know about your case is your brief summary... >If Toprol is the only try at medical management that you've had, you should investigate other drugs. But in any case, it appears that you and your cardiologist are not a good match. Find someone else. Answered by Lonnie Papka 1 year ago.

conventional untimely ventricular contractions. %. originate whilst another part of the middle (in the ventricles) than it relatively is organic heartbeat inititator initiates a beat. Answered by Analisa Zaharek 1 year ago.


Why does the bronchodilator exaggerate the tachycardia?
Asked by Caron Vogtman 1 year ago.

Bronchodilators were originally alpha or beta agonists. The grandfather of all of them is epinephrine.(Norepinephrine was primarily an alpha agonist and used mostly to treat kids with Croup.) Both of which would relax the bronchial muscles but had the side effect of increasing the heart rate. Through research it was found the the beta receptors were of two types, Beta 1 and beta 2. Beta 1 increased the heart rate while beta 2 relaxed the bronchial muscles. The pharmaceutical companies further refined the epinephrine to stimulate only the beta 2 receptors. They also refined it to block the beta 1 effects becoming the class of drugs known as beta blockers.This was used in tachyarrythmnias. Isuprel was the first beta agonist and it was very effective and fast acting but there was still a lot of beta 1 activity. Then came Bronkosol(Isoetharine) which seemed to have solved the problem. Alupent was next. Finally Albuterol was introduced which had virtually no beta 1 activity. The onset of activity was longer(up to 5 min.) but the effect on heart rate was much less. Some people still get an increase in heart rate with Albuterol but the percentage is very small. You still have to monitor the patient for heart rate increase but the likelihood is much less. I should have explained at the beginning that there are two types of nerves in the peripheral nervous system. Sympathetic and parasympathetic. While one has one effect the other has the opposite effect. Epinepherine is a sympathomimetic or "mimics" the sympathetic nerves. A drug which stimulates the parasympathetic system would be a parasympathomimetic. Any drug that reduces the effect of one of these is said to "lyse" the effect. So a drug which reduced the parasympathetic system would be called a parasympatholytic. The sympathetic system dilates or relaxes the bronchial muscles and the parasympathetic system constricts them. If you were to give a sympathomimetic and a parasympatholytic at the same time you would be attacking the problem from two sides. Atrovent is a parasympatholytic drug often given with Albuterol and is called Combivent. Studies have shown that in certain patients the bronchodilator effect is enhanced by the addition of Atrovent. God bless. Answered by Chana Sorrentino 1 year ago.

because it has beta 1 receptor effect at the heart...which when stimulated caused an increased in heart beat Answered by Georgiann Quammen 1 year ago.


Why should one use a bronchodilator before a corticosteroid?
A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first,... Asked by Emory Tritto 1 year ago.

A Bronchodilator opens up the airway so that the steroid can travel deeper into the lungs to clear the inflammation. Bronchodilators open up and relax constricted airways making it easier to breathe. Steroids are used to reduce inflammation and swelling in the airways. Hence why we use the bronchodilator first, then the steroid inhaler. -Rekha, RN/BSN Answered by Alverta Weygandt 1 year ago.

Bronchodilators work systemically. They have no local effect. It's absorbed into the mucosa and thereby the blood vessels. Don't forget it has to be absorbed through the mucous layer and then the inflamed mucosa before it gets anywhere near the bronchial musculature. And, being Beta 2 agonists they only relax the bronchial muscles. They do not relieve inflammation. The saline is a mucolytic and works faster and locally. Of course, this is when you are taking the unit dose. If you are using the metered dose inhaler (MDI) there is no saline so it's best to wait 5 minutes for the full effect before taking the steroid. Once you cough the mucous out the bronchodilator can get to the membrane and be absorbed into the circulation faster. It is doing no good being absorbed by the mucous itself. Albuterol is the chemical evolutionary end product of epinephrine for the relief of bronchospasm. Epinephrine, of course, has primarily beta 1 and beta 2 effects. and it's very fast acting but it only lasts for maybe an hour. Isuprel was the next step. It's onset of effect was about 2 minutes but it remained effective for about two hours and the dose, as with epinephrine, had to be titred to the patient's heart rate. Bronkosol was the next in line. It's peak effect was achieved in 3-4 minutes but only lasted 3 hours. Alupent was about the same. Albuterol achieves it's maximum effect in 5 minutes and lasts for about 4 hours. All these meds were created in an attempt to mitigate the cardiac side effects by making them less beta 1 and more beta 2 agonists. Norepinephrine is primarily an alpha agonist and used, in titred doses, for acute laryngotracheobronchitis in children providing a fast acting anti inflammatory. Now once the bronchodilator is absorbed you can get maximum penetration of the steroid for it's localized effect on the inflammation and swelling. Also, a good tip is, if you are ordered to take two puffs from the MDI, wait 5 minutes between puffs so you get maximum effect from the first puff and the second one will get deeper. I know it's hard to wait but I always told my patients this and they all remarked what a difference it makes. Answered by Romaine Madonna 1 year ago.

Because if you relax and open the airways first, then the steriod can better penetrate the lungs to reduce inflammation. Answered by Clementina Mckibbens 1 year ago.

ASKED AND ANSWERED. THANKS FOR THE POINTS! Answered by Ezequiel Vicent 1 year ago.


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