EpiPen Question

[medichopeful]

I had a relatively weird conversation last night, and after thinking it over, I'd love to ask for some opinions, clarification, etc..

I was talking medicine with somebody, and they mentioned that they had an EpiPen, which was no big deal. But then they mentioned that they were told (by their doctor) that if their heart stopped, or they needed to have an AED used on them, that they should first be injected with their EpiPen, THAN they should be shocked.

My response was, "what?!" Granted, I'm no doctor (but I have SO much knowledge from EMT-B class that I should just be made an honorary doctor ), but there seems to be something not quite right about this.

This person says that their cardiologist gave them the pen and said to use it (or have somebody else use it) in a case like that. It could also be used for an allergic reaction. This person does have a heart condition, and they said something about their adrenaline being maxed-out, so they would need to have a little more put into them to actually restart their heart.

I thought, however, that the epinephrine used for allergic reactions and cardiac arrest were different (1:1000 for an allergic reaction, 1:10000 for cardiac arrest). Is this correct? Without any more information, could anybody educate me on this, or cite an article describing it? I'm really confused by this, and I want to learn more.

Thanks!
Eric

 

[Lifeguards For Life]

http://www.emtlife.com/showthread.php?t=13039

the concentration in an epi pen is 1:1000 not 1:10000 as you mentioned. Think about all the anatomical barriers the epi has to cross if injected into a muscle as opposed to straight into the blood stream. On top of this the patient is dependant on your compressions to circulate the drug.

I believe the epi auto injector also has half the dose of what would be administered in cardiac arrest.

 

[medichopeful]

http://www.emtlife.com/showthread.php?t=13039

the concentration in an epi pen is 1:1000 not 1:10000 as you mentioned. Think about all the anatomical barriers the epi has to cross if injected into a muscle as opposed to straight into the blood stream. On top of this the patient is dependant on your compressions to circulate the drug.

I believe the epi auto injector also has half the dose of what would be administered in cardiac arrest.

You know what? I actually remember seeing that thread. :blush:

I was pretty confused by the whole thing. I looked at the EpiPen, and it specifically said "for allergic reactions" (or something similar). I'm really confused by why she thought this. I'll have to talk to her about it next time I see her and try to clear the whole thing up :wacko:

 

[dave3189]

BTW, he didn't say that an Epi pen was 1:10000, he said it was 1:1000 for an allergic reaction and 1:10000 for C.A.

 

[MusicMedic]

I had a relatively weird conversation last night, and after thinking it over, I'd love to ask for some opinions, clarification, etc..

I was talking medicine with somebody, and they mentioned that they had an EpiPen, which was no big deal. But then they mentioned that they were told (by their doctor) that if their heart stopped, or they needed to have an AED used on them, that they should first be injected with their EpiPen, THAN they should be shocked.

My response was, "what?!" Granted, I'm no doctor (but I have SO much knowledge from EMT-B class that I should just be made an honorary doctor ), but there seems to be something not quite right about this.

This person says that their cardiologist gave them the pen and said to use it (or have somebody else use it) in a case like that. It could also be used for an allergic reaction. This person does have a heart condition, and they said something about their adrenaline being maxed-out, so they would need to have a little more put into them to actually restart their heart.

I thought, however, that the epinephrine used for allergic reactions and cardiac arrest were different (1:1000 for an allergic reaction, 1:10000 for cardiac arrest). Is this correct? Without any more information, could anybody educate me on this, or cite an article describing it? I'm really confused by this, and I want to learn more.

Thanks!
Eric

She probably was misinformed or Misunderstood that Epi is used for Asystole/PEA rather than V-fib
because alot of people who dont know much about medicine generally think Heart-Attack=Heart Stopping, on top of that alot of people who arnt in medicine think that you can Shock a Cardiac Arrest

so i think its more of the person you are talking to Misunderstanding

 

[Lifeguards For Life]

She probably was misinformed or Misunderstood that Epi is used for Asystole/PEA rather than V-fib
because alot of people who dont know much about medicine generally think Heart-Attack=Heart Stopping, on top of that alot of people who arnt in medicine think that you can Shock a Cardiac Arrest

so i think its more of the person you are talking to Misunderstanding

Epi is indicated for v-fib.

v-fib and pulse less v-tach are both presentations of cardiac arrest, and they both need be defibrillated.
:unsure:

 

[MusicMedic]

Epi is indicated for v-fib.

v-fib and pulse less v-tach are both presentations of cardiac arrest, and they both need be defibrillated.
:unsure:

Oh intresting, i didnt know that lol, oh maybe i did i just forgot haha

how would Epi help on a v-fib?

 

[Lifeguards For Life]

Oh intresting, i didnt know that lol, oh maybe i did i just forgot haha

how would Epi help on a v-fib?

In ventricular fibrillation there is no organized depolarization of the ventricles. the ventricles just "quiver". consequently there is no effective myocardial contraction, hince no pulse.

While no drugs have actually been shown to improve survival to hospital discharge a vasopressor is still indicated in the v-fib and pulseless v-tach algorithms.

The vasopressor is either epi or vasopressin, preferably epi.

Epi is preferable because it stimulates a1, b1, and b2 receptors.

As an alpha antagonist epi constricts arteries and arterioles systemically, leading to increased systemic vascular resistance, which will help to make compressions more effective.

As a beta1 antagonist epi has a positive inotropic effect, positive chronotropic effects. this means that the force of contractions and oxygen requirements of the heart will actually be increased.

As a beta2 antagonist epi relaxes smooth muscle in the bronchials, and dilate vessels in the cerebral, pulmonary, coronary, and hepatic vessels. this will help offset the increased demands from the beta1 effects.

 

[Shishkabob]

Epinephrine is epinephrine. 1:1,000 and 1:10,000 are just the concentration of the medicine.

1:1 has 1mg of Epi in 1ml of solvent, while 1:10 has 1mg of epi in 10ml of solvent.


Epi 1:1 and 1:10 are BOTH used in allergic reactions. The difference between the two is the route it is given to the body. 1:1 is given SQ and IM, while 1:10 is given IV. If 1:1 is given IV it causes massive amounts of vasoconstriction.


Epi in allergic reactions tend to be in the .3-.5mg dose range for both 1:1 and 1:10. Epi for cardiac arrest is 1mg 1:10

The vasopressor is either epi or vasopressin, preferably epi.

Epi is preferable because it stimulates a1, b1, and b2 receptors.

Vasopressin last longer and in some studies, better survival rates (to admission).

And we don't care much about B2 receptors in cardiac arrest.

PS- They are agonist, not antagonist

 

[Lifeguards For Life]

Epinephrine is epinephrine. 1:1,000 and 1:10,000 are just the concentration of the medicine.

1:1 has 1mg of Epi in 1ml of solvent, while 1:10 has 1mg of epi in 10ml of solvent.


Epi 1:1 and 1:10 are BOTH used in allergic reactions. The difference between the two is the route it is given to the body. 1:1 is given SQ and IM, while 1:10 is given IV. If 1:1 is given IV it causes massive amounts of vasoconstriction.


Epi in allergic reactions tend to be in the .3-.5mg dose range for both 1:1 and 1:10. Epi for cardiac arrest is 1mg 1:10

what about epi 1:2?

when does it come into play?

 

[Shishkabob]

what about epi 1:2?

when does it come into play?

When you're woken up at 3am and have to mix your own 1:10 and grab the wrong syringe

 

[MusicMedic]

In ventricular fibrillation there is no organized depolarization of the ventricles. the ventricles just "quiver". consequently there is no effective myocardial contraction, hince no pulse.

While no drugs have actually been shown to improve survival to hospital discharge a vasopressor is still indicated in the v-fib and pulseless v-tach algorithms.

The vasopressor is either epi or vasopressin, preferably epi.

Epi is preferable because it stimulates a1, b1, and b2 receptors.

As an alpha antagonist epi constricts arteries and arterioles systemically, leading to increased systemic vascular resistance, which will help to make compressions more effective.

As a beta1 antagonist epi has a positive inotropic effect, positive chronotropic effects. this means that the force of contractions and oxygen requirements of the heart will actually be increased.

As a beta2 antagonist epi relaxes smooth muscle in the bronchials, and dilate vessels in the cerebral, pulmonary, coronary, and hepatic vessels. this will help offset the increased demands from the beta1 effects.

Thats why your on your way to becoming a Paramedic

I learn something more in dept everyday on this forum

you medic students are oh so knowledgeable about pharmacology, i cant wait to be in your shoes!!!!!!

i wish i took some Pharm Classes along with my EMT class

 

[Lifeguards For Life]

When you're woken up at 3am and have to mix your own 1:10 and grab the wrong syringe

The epipen brand epi pen junior auto injectors contain 2ml of epi 1:2000.

Only reason i know is i saw 1:2000 in the PDR and it stuck out to me

 

[Lifeguards For Life]

PS- They are agonist, not antagonist

second time i've done that:glare:

yes, it should of read agonist not antagonist...

 

[Fedekz]

http://www.emtlife.com/showthread.php?t=13039

the concentration in an epi pen is 1:1000 not 1:10000 as you mentioned. Think about all the anatomical barriers the epi has to cross if injected into a muscle as opposed to straight into the blood stream. On top of this the patient is dependant on your compressions to circulate the drug.

I believe the epi auto injector also has half the dose of what would be administered in cardiac arrest.

The epi pen has .3 mg of epi. The cardiac arrest dose is 1 mg epi 1:10 q 5.

 

[Veneficus]

Vasopressin last longer and in some studies, better survival rates (to admission).

And we don't care much about B2 receptors in cardiac arrest.

Just want to comment on short term survival compared to survival to discharge for your consideration.

In sudden cardiac death, by various mechanisms I am too lazy to type today, the wall of the heart is weakened between 1-10 days (most common 3-10 depending on who you ask/read) by coagulative necrosis and the macrophage absorbtion and neutophil lysis of the myocardial connective tissue resulting in free wall rupture. (most commonly the ventricular septum)

The increased risk factors for this is also a considerable list, but a few (incomplete) are: female, persons without ventricular hypertrophy, age greater than 60.

Since the wall rupture and subsequent death are part of the body's immune and healing response to the event and not during the emergent stage, medications that improve survival to admission possibly give the patient a chance to survive the initial stages of the event they would not have had should they not survive the initial resuscitation of a relevant pathology.

Just something to think about.

almost forgot, the central vasodilaton effects of epi do hold some benefit, so while not of primary concern for the airway, the B2 stimulation does play a role.

 

[Smash]

almost forgot, the central vasodilaton effects of epi do hold some benefit, so while not of primary concern for the airway, the B2 stimulation does play a role.

I would be interested to see references for this. My understanding of the Beta effects of epi in cardiac arrest is that they are all deleterious (hence the interest in vasopressin as a pure alpha agonist, specifically alpha2).

IV epi is associated with increased myocardial workload and O2 demand; increased incidence of arrythmia; decreased ability of the heart to relax (negative lusiotrope); increased shunt from decreased hypoxic pulmonary vasoconstriction; increased incidence of post-resuscitation myocardial dysfunction and increased post-resuscitation cerebral dysfunction. Essentially all of these negatives are associated with the beta effects (although some are related to alpha-adrenergic modulated microvascular dysfunction in the brain and maybe the heart - selective alpha2 agents may be the way to go for that...may)

Ok, some references, taken as a large lump from the first bibliographic I could find on my cluttered and straining hard-drive - some may not be entirely relevant sorry. It is late and I am tired (also sorry about the formatting)

Achleitner, U., Wenzel, V., Strohmenger, H. U., Krismer, A. C., Lurie, K. G., Lindner, K. H., et al. (2000). The effects of repeated doses of vasopressin or epinephrine on ventricular fibrillation in a porcine model of prolonged cardiopulmonary resuscitation. Anesth Analg, 90(5), 1067-1075.

Adgey, A. A. (1998). Adrenaline dosage and buffers in cardiac arrest. Heart, 80(4), 412-414.

Angelos, M. G., Butke, R. L., Panchal, A. R., Torres, C. A., Blumberg, A., Schneider, J. E., et al. (2008). Cardiovascular response to epinephrine varies with increasing duration of cardiac arrest. Resuscitation, 77(1), 101-110.

Angelos, M. G., & DeBehnke, D. J. (1995a). Epinephrine-mediated changes in
carbon dioxide tension during reperfusion of ventricular fibrillation in a canine model. Crit Care Med, 23(5), 925-930.

Angelos, M. G., & DeBehnke, D. J. (1995b). Epinephrine and high-flow reperfusion after cardiac arrest in a canine model. Ann Emerg Med, 26(2), 208-215.

Angelos, M. G., Torres, C. A., Waite, M. D., Rath, D. P., Zhu, H., Beckley, P. D., et al. (2000). Left ventricular myocardial adenosine triphosphate changes during reperfusion of ventricular fibrillation: the influence of flow and epinephrine. Crit Care Med, 28(5), 1503-1508.

Babar, S. I., Berg, R. A., Hilwig, R. W., Kern, K. B., & Ewy, G. A. (1999). Vasopressin versus epinephrine during cardiopulmonary resuscitation: a randomized swine outcome study. Resuscitation, 41(2), 185-192.

Berg, R. A., Otto, C. W., Kern, K. B., Sanders, A. B., Hilwig, R. W., Hansen, K.
K., et al. (1994). High-dose epinephrine results in greater early mortality after resuscitation from prolonged cardiac arrest in pigs: a prospective, randomized study. Crit Care Med, 22(2), 282-290.

DeBehnke, D. J., Angelos, M. G., & Leasure, J. E. (1992). Use of
cardiopulmonary bypass, high-dose epinephrine, and standard-dose epinephrine in resuscitation from post-countershock electromechanical dissociation. Ann Emerg Med, 21(9), 1051-1057.

Ditchey, R. V., & Lindenfeld, J. (1988). Failure of epinephrine to improve the balance between myocardial oxygen supply and demand during closed-chest resuscitation in dogs. Circulation, 78(2), 382-389.

Huang, L., Sun, S., Fang, X., Tang, W., & Weil, M. H. (2006). Simultaneous blockade of alpha1- and beta-actions of epinephrine during cardiopulmonary resuscitation. Crit Care Med, 34(12 Suppl), S483-485.

Kern, K. B. (2002). Postresuscitation myocardial dysfunction. Cardiol Clin, 20(1), 89-101.

Klouche, K., Weil, M. H., Sun, S., Tang, W., & Zhao, D. H. (2003). A comparison of alpha-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation. Resuscitation, 57(1), 93-100.

Krismer, A. C., Hogan, Q. H., Wenzel, V., Lindner, K. H., Achleitner, U., Oroszy, S., et al. (2001). The efficacy of epinephrine or vasopressin for resuscitation during epidural anesthesia. Anesth Analg, 93(3), 734-742.

Krismer, A. C., Lindner, K. H., Kornberger, R., Wenzel, V., Mueller, G., Hund, W., et al. (2000). Cardiopulmonary resuscitation during severe hypothermia in pigs: does epinephrine or vasopressin increase coronary perfusion pressure? Anesth Analg, 90(1), 69-73.

Lindner, K. H., Ahnefeld, F. W., Bowdler, I. M., & Prengel, A. W. (1991). Influence of epinephrine on systemic, myocardial, and cerebral acid-base status during cardiopulmonary resuscitation. Anesthesiology, 74(2), 333-339.

Lindner, K. H., Ahnefeld, F. W., Schuermann, W., & Bowdler, I. M. (1990). Epinephrine and norepinephrine in cardiopulmonary resuscitation. Effects on myocardial oxygen delivery and consumption. Chest, 97(6), 1458-1462.

Lindner, K. H., Strohmenger, H. U., Prengel, A. W., Ensinger, H., Goertz, A., & Weichel, T. (1992). Hemodynamic and metabolic effects of epinephrine during cardiopulmonary resuscitation in a pig model. Crit Care Med, 20(7), 1020-1026

Little, C. M., Angelos, M. G., & Paradis, N. A. (2003). Compared to angiotensin II, epinephrine is associated with high myocardial blood flow following return of spontaneous circulation after cardiac arrest. Resuscitation, 59(3), 353-359.

Loeckinger, A., Kleinsasser, A., Wenzel, V., Mair, V., Keller, C., Kolbitsch, C., et al. (2002). Pulmonary gas exchange after cardiopulmonary resuscitation with either vasopressin or epinephrine. Crit Care Med, 30(9), 2059-2062.

Ristagno, G., Sun, S., Tang, W., Castillo, C., & Weil, M. H. (2007). Effects of epinephrine and vasopressin on cerebral microcirculatory flows during and after cardiopulmonary resuscitation. Crit Care Med, 35(9), 2145-2149.

Ristagno, G., Tang, W., Huang, L., Fymat, A., Chang, Y. T., Sun, S., et al. (2009). Epinephrine reduces cerebral perfusion during cardiopulmonary resuscitation. Crit Care Med, 37(4), 1408-1415.

Stiell, I. G., Hebert, P. C., Wells, G. A., Vandemheen, K. L., Tang, A. S., Higginson, L. A., et al. (2001). Vasopressin versus epinephrine for inhospital cardiac arrest: a randomised controlled trial. Lancet, 358(9276), 105-109.

Sutton, R. M., Berg, R. A., & Helfaer, M. A. (2009). Epinephrine for resuscitation from cardiac arrest: A double-edged sword? Crit Care Med, 37(4), 1518-1520.

Tang, W. (2000). Use of epinephrine as vasopressor agent during cardiopulmonary resuscitation: another example of a double-edged sword. Crit Care Med, 28(5), 1671-1672.

Tang, W., Weil, M. H., Sun, S., Gazmuri, R. J., & Bisera, J. (1993). Progressive myocardial dysfunction after cardiac resuscitation. Crit Care Med, 21(7), 1046-1050.

Tang, W., Weil, M. H., Sun, S., Noc, M., Yang, L., & Gazmuri, R. J. (1995). Epinephrine increases the severity of postresuscitation myocardial dysfunction. Circulation, 92(10), 3089-3093.

Voelckel, W. G., Lindner, K. H., Wenzel, V., Bonatti, J., Hangler, H., Frimmel, C., et al. (2000). Effects of vasopressin and epinephrine on splanchnic blood flow and renal function during and after cardiopulmonary resuscitation in pigs.
Crit Care Med, 28(4), 1083-1088.

Voelckel, W. G., Lurie, K. G., McKnite, S., Zielinski, T., Lindstrom, P., Peterson, C., et al. (2002). Effects of epinephrine and vasopressin in a piglet model of prolonged ventricular fibrillation and cardiopulmonary resuscitation. Crit Care Med, 30(5), 957-962.

Wenzel, V., Krismer, A. C., Arntz, H. R., Sitter, H., Stadlbauer, K. H., & Lindner, K. H. (2004). A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med, 350(2), 105-113.

Wenzel, V., & Lindner, K. H. (2006). Vasopressin combined with epinephrine during cardiac resuscitation: a solution for the future? Crit Care, 10(1), 125.

 

[Veneficus]

I would be interested to see references for this. My understanding of the Beta effects of epi in cardiac arrest is that they are all deleterious (hence the interest in vasopressin as a pure alpha agonist, specifically alpha2).

IV epi is associated with increased myocardial workload and O2 demand; increased incidence of arrythmia; decreased ability of the heart to relax (negative lusiotrope); increased shunt from decreased hypoxic pulmonary vasoconstriction; increased incidence of post-resuscitation myocardial dysfunction and increased post-resuscitation cerebral dysfunction. Essentially all of these negatives are associated with the beta effects (although some are related to alpha-adrenergic modulated microvascular dysfunction in the brain and maybe the heart - selective alpha2 agents may be the way to go for that...may)

It is my understanding that the Beta 2 stimulation in central circulation helps to reduce the alpha 1 vasoconstriction that reduces coronary blood supply. whether or not this helps in long term survival I have no idea, but based purely on the basic science, it should help. In evidence I respectfully submit:

http://jtcs.ctsnetjournals.org/cgi/content/full/118/3/446

It is not specific to cardiac arrest, however it is specific to Beta reception in the heart.

I looked through 5 or 6 of the studies you posted as well as spent some time doing my own search on the web this morning. I am not sure from these studies how you come to such a definitive conclusion that all Beta stimulation is deletorious.

Many of the studies are attempting to compare standard vs. high dose epi. (which to my underdtanding has largely been eliminated except in a very small subset of patients)

Others are focusing directly on the peripheral vascular resistance aspects of vasopression vs. epi or in conjunction. All of the studies I went through from your post stated there was an increase in short term survival with vasopressin in PEA and asystole , but survival to discharge was unchanged.

In retrospect I probably should have softened my statement of there are beneficial effects of beta stimulation to there may be beneficial effects, but in my defense I did limit the position to beta 2 receptors.

For furhter published discussion, I submit:

http://circ.ahajournals.org/cgi/content/full/112/24_suppl/IV-58

additionally here is link to another source that is quoted that basically repeats the same thing:

http://www.nurse-anesthesia.org/showthread.php?t=1955

The only overwhelming consensus I could find in your sources or my search was that the compound effects of total beta stimulation may be more harmful than beneficial, but nobody took the opinion that it was absolute, and much of the language looked more neutral to me.

There was consensus that there are competing schools of thought as to whether or not Epi is benefical or harmful and neither was conclusive.

In support of your position, I did see one study that showed in hospital arrests treated with epi had a significant higher amount of negative outcomes. But the same study stipulated there was no difference in out of hospital outcome.

As well, the studies showing treatment with combined beta blocker therapy and epi also did not have any significant change on short or longterm outcome.

(I hope you don't mind I didn't repost the links as all except the links I did post, came from your sources)

I admit i didn't go through them all, but I did the top 2 and some random ones in the list.