tchristifulli
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So how much do you think Epi will be effected when given for anaphylaxis in a person who takes Beta Blockers on a regular basis ?
Epinephrine administration to people on Beta Blockers
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I read of a case somewhere where glucagon had to be administered before the Epi was able to reach the desired effect. I'll see if I can find it.
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Now my understanding of Glucagon's role in Beta Blocker overdoses is that it doesn't reverse the effects of the Beta Blocker as much as it bypasses the adrenergic messenger system and increases cAMP by a secondary Ca ++ influx. I would love to see that article though!
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That's my understanding as well. I'll see if I have it saved on my laptop when I get home in the morning
mycrofft
Still crazy but elsewhere
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I take beta blockers for AFib. Even before I was diagnosed the epi in dental local anesthesia would give me a "tight chest" sensation. Gulping a 20 oz Mt Dew noticeably raises my heart rate. It may vary from person to person, but as for me, find something else please.
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tchristifulli
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I've heared of Glucagon being administered to people on beta blockers who are having an allergic reaction, but I thought that was due to glucagon being a smoothe muscle relaxer and helping dilate the bronchioles.
blindsideflank
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^^^ but how?
im trying to find a good pic of a cell membrane with a beta receptor, and calcium channel that will show how/why glucagon and phosphodiesterase inhibitors work
standby im not good at the internet. i wish i could scan my books
im trying to find a good pic of a cell membrane with a beta receptor, and calcium channel that will show how/why glucagon and phosphodiesterase inhibitors work
standby im not good at the internet. i wish i could scan my books
Christopher
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Glucagon exhibits similar effects to beta agonists due to its signalling of the c-AMP pathways. This is orthogonal to the beta adrenergic system, hence it is not affected by B-blockers. It has a wider profile than just bronchodilation. I looked at some of these additional profiles in a review of glucagon I wrote.
Nebulized glucagon theoretically provides bronchodilation, however, there is very little evidence to support this practice.
IV glucagon will provide inotropic and chronotropic support at sufficient dosages, and while there is some tiny literature support, it isn't exactly The Gold Standard.
The honest answer is you're probably better off working through increasing dosages of your typical sympathomimetics first. A recent review of vasopressors for Ca-channel blocker OD's (arguably worse than a B-blocker problem) had dosing 10x the usual EMS maximums.
MagicTyler
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The amount of glucagon in an ambulance isn't going to do much to help. I saw a beta blocker overdose come into the ED (he had taken 3 pills instead of 1) and the ED doc used all of the available glucagon in the hospital with little affect.
Beta 1 and beta 2 receptors use G-protein receptors that activate adenylate cyclase, which produces cAMP, which then goes and does what it does depending on the cell. Alpha-1 receptors stimulate a different type of G-protein receptor that results the production of DAG and IP3, which then, generally, activates protein kinase C and the initiate the release of Ca from the sarcoplasmic reticulum, respectively. This will lead to smooth muscle contraction.
And yeah, regardless, it will take a lot of glucagon to reverse beta-blocker (or CCB) ODs. Also, insulin is a positive inotrope, but I think that has more to do with calcium movement from the sarcoplasmic reticulum or from outside the cell.
Phosphodiesterase inhibitors, inhibit phosphodiesterase (duh), which is responsible for the breakdown of cGMP in smooth muscle cells. cGMP phosphorylates myosin light chain kinase, inactivating it so that it cannot phosphorylate myosin, which would cause smooth muscle contraction. (cAMP does the same/similar.)
Thats what I recall off the top of my head (ok, with a couple quick glances at a diagram). Someone correct my mistakes.
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Anyone on a beta blocker will probably be resistant to epinephrine to some degree. How resistant they are probably depends on which beta blocker they are on, how large of a dose they are on, and how long they've been taking it.
Resistance isn't the only thing to worry about when giving epi to someone who is beta blocked, though. You can get profound hypertension if someone taking the non-cardioselective beta blockers receives epi. This is because epi has both Alpha (constricting) and Beta (dilating) effects on vascular smooth muscle. Normally they cancel each other out to a pretty good degree. But a non-selective beta blockers will block the Beta (dilating) effects of epi, which means there is nothing to offset the Alpha (vasoconstrictive) effects. The net result can be a massive increase in SVR (afterload), with the heart unable to increase stroke volume enough to compensate (since the heart is not beta blocked), and causing a severe decrease in systemic perfusion. This is the same reason beta blockers are avoided in someone who is toxic on cocaine or another stimulant.
If someone is on the cardioselective (B1) beta blockers - which seem more common these days - you don't get that effect because the the vasodilatory effects of epi are not blocked.
Someone who is on beta blockers for hypertension, angina, or post- MI is more likely on a cardio-selective (B1-specific) BB, such as atenolol or metoprolol. If they are on the BB for anxiety or migraines, they may be on a non-selective drug.
The ones you really need to watch out for as far as resistance goes is those on both alpha blockers and beta blockers.
mycrofft
Still crazy but elsewhere
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Just switch from missiles to guns....give antihistamine.
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tchristifulli
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I thought EPI only dilated the bronchioles. I've never heared of it dilating the vessels as well?
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It primarily constricts. Coronary arteries are relaxed, though, and there's some evidence that cerebral arteries are dilated as well.
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Like Halothane said, Epinephrine has both Alpha and Beta effects in vivo. Beta receptors are involved in smooth muscle vasodilation, but are primarily offset by Alpha vasoconstriction. Epinephrine is extremely non-selective and exhibits effects on all types of Alpha and Beta receptors.
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Are we talking about selective or non-selective beta blockers?
Sorry, had to ask.
Sorry, had to ask.
Beta-2 receptors are found in (nearly) all smooth muscle - includes smooth muscles in the vasculature, GI tract, bladder, and uterus. And the result of beta-2 stimulation is some degree of smooth muscle relaxation. Isoproterenol, which some may have seen used, is a potent beta-1 and beta-2 agonist. It has virtually no alpha activity. Despite the chrono- and inotropic effects on the heart, it typically will lower the blood pressure due to vasodilation in the periphery. Terbutaline, which is beta-2 agonist, is frequently used to decrease uterine contraction in pre-term labor (and you can use albuterol, too).
Under general physiologic condition, it is believed that local mediators have far greater control over vascular tone: e.g. nitric oxide (muscle and skin) or adenosine (coronary arteries).
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Just had to make a correction to my original post.
Apparently the edit option is no longer available?
Apparently the edit option is no longer available?
NomadicMedic
I know a guy who knows a guy.
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Huh.
Before I became a premium member, I'd occasionally look back over past posts and edit typos and grammar, and sometimes that was days after I originally posted. In fact just a few days ago, I was able to edit typos in a post I made weeks ago.
I just recently became a premium member, and this is the first time I've tried to edit a post and was unable to.