ACLS - Do's and Don't?

[Scout]

Ok but if I'm off base here do tell. I haven't researched this it is mere personal opinion.


My understanding of O2 in those instances was that it relieved pain due to an effect on an underlying condition or a change of state occurs. This contrasts in with other pain relief as the pain relief we give does nothing for the the cause but depressant for the signals so you don't feel it.

Also I have found, all be it limited, that if you apply o2, and I'm assuming compressed air will work too, the pt often reports a decrease in pain. Coupled if you tell them it will help with the pain it helps quite a bit.

 

[VentMedic]

Ok but if I'm off base here do tell. I haven't researched this it is mere personal opinion.


My understanding of O2 in those instances was that it relieved pain due to an effect on an underlying condition or a change of state occurs. This contrasts in with other pain relief as the pain relief we give does nothing for the the cause but depressant for the signals so you don't feel it.

Also I have found, all be it limited, that if you apply o2, and I'm assuming compressed air will work too, the pt often reports a decrease in pain. Coupled if you tell them it will help with the pain it helps quite a bit.

Again, oxygen is a drug, not a placebo, regardless of the quantity you give it. It you are giving compressed air, you may still be providing a therapy. The flow itself is therapeutic. It is not like you are giving a placebo pill.

CPAP at 21% can relieve alot of symptoms and it is from the mechanism of delivery that improves oxygen uptake. It there is a V/Q mismatch, varying flow gradients can make a big improvement. Thus, there are many basic priniciples that must be understood before making a blanket statement or the common EMS thing "I have seen this" but without any information to support their claim.

 

[VentMedic]

I am going to continue a little further with this.

This is my post from the CP and O2 thread:
Oxygen, oxidative stress, hypoxia, and heart failure

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15765131

Conclusions
Oxygen, beyond its indispensable role in cardiac energy metabolism, plays a central role in other biological processes that can be determinants of cardiac function, including the generation of ROS and the determination of cardiac gene expression patterns. Although their role in the pathogenesis of clinical heart failure remains unclear, ROS have been implicated in most processes thought to have a significant effect on cardiac function, including hypertrophy, ion flux and calcium handling, EC coupling, extracellular matrix configuration, vasomotor function, metabolism, gene expression, and downstream signaling of several growth factors and cytokines. Clinical trials based on antioxidant therapies have been, however, generally disappointing. Whether this is a function of the particular antioxidants used is unclear, and planned trials with XO inhibitors and other alternative agents should help answer this question. The role of hypoxia-induced alterations in gene expression in the genesis of heart failure also remains unclear, although experimental data suggest that these changes in gene expression can be either adaptive or maladaptive, depending on context. Given the central role of oxygen in cardiovascular biology, further investigational focus on oxygen-related processes in the genesis of heart failure is warranted.

The research indicates that Oxygen does produce various changes in the body and that is why its use in different concentrations of various lengths of time is controversial.

We also know that various ethnic groups do have some differences in their cellular chemistry that make them susceptible to different diseases and they may also response to different therapies better or poorer than other races.

ex. The Asian or African-American race have a higher risk for Pulmonary Artery Hypertension due to a nitric oxide deficiency. They are also at a higher risk for asthma. Sickle cell trait and O2 carrying capacity will also be factors. Different treatment plans must take this into consideration. Thus, medications and therapies must take into consideration many factors and what you may perceive as a placebo effect may actually have some physiological effect on that particular person and not on another.

You can use the intake of everyday vitamins as an example. If your body doesn't need the supplements, they are of little use and are excreted. If your body is deficient in something, then the may serve a purpose.

 

[maxwell]

Oxygen is required to generate ATP as a source of cellular chemical energy. Without it, the Kreb's cycle does not function and some system may suffer, causing pain.

I suggest a little basic college level A&P to review the principles of Oxygen and why it is considered a drug.

I'll be sure to mention this to the biochem class I'm TAing this semester. Note: The big payoff for ATP isn't during the Krebs cycle..its the electron transport chain where O2 is the final oxygen acceptor. Moreover, pain is generally not due to a lack of A3P! And while all of this is really, really interesting... Oxygen as a pain relief is goofy! Oxygen, of course, when pain is due to hypoxia, helps in the long run. Pain mgmt should focus on early delivery of narcotics and consideration of anxiolytics. We don't give O2 for pain, we give it to prevent systemic hypoxia (which can THEN lead to issues at the biochemical level).

 

[JPINFV]

Note: The big payoff for ATP isn't during the Krebs cycle..its the electron transport chain where O2 is the final oxygen acceptor.

True, to an extent. While Krebs only produces one unit of GTP per cycle (2 cycles per unit of glucose that enters glycolysis), it does produce 3 units of NADH which is needed to run the electron transport chain. If ETC backs up (for example cyanide poisoning or hypoxia), then the cell will run out of free NAD+ which will shut down the Krebs cycle.

 

[VentMedic]

I'll be sure to mention this to the biochem class I'm TAing this semester. Note: The big payoff for ATP isn't during the Krebs cycle..its the electron transport chain where O2 is the final oxygen acceptor. Moreover, pain is generally not due to a lack of A3P! And while all of this is really, really interesting... Oxygen as a pain relief is goofy! Oxygen, of course, when pain is due to hypoxia, helps in the long run. Pain mgmt should focus on early delivery of narcotics and consideration of anxiolytics. We don't give O2 for pain, we give it to prevent systemic hypoxia (which can THEN lead to issues at the biochemical level).

Again I would suggest some college level A&P to see how systems are related and further your studies. You are taking small pieces of info out of context of a bigger picture. After you finish the Biochemistry class you should have a better understanding of this. But, is this an "overview" class? If this is a regular college level Biochem class, you should have gotten more information in the prerequisite classes.

If you have college level classes to your credit, especially in the sciences, you would know why making a blanket statement like this:

Originally Posted by maxwell
..oxygen does nothing for pain.

is invalid. Support your statements.

I have given you examples and you can do your own research.

Here are two decent search engines to look for medical literature.

www.medscape.com

http://scholar.google.com/

We don't give O2 for pain, we give it to prevent systemic hypoxia

This applies only to an EMT or Paramedic level. Once again there is much more to medicine off the ambulances.

 

[maxwell]

I'll leave the previous statements be as it will have no benefit to pt. care. I just put "oxygen, pain" into NIHP-M, and got plenty of support for my statements. O2 15L for pain, for all! Oh, and I'm teaching the biochem class. I'm good with my "big picture."

 

[VentMedic]

I'll leave the previous statements be as it will have no benefit to pt. care. I just put "oxygen, pain" into NIHP-M, and got plenty of support for my statements. O2 15L for pain, for all! Oh, and I'm teaching the biochem class. I'm good with my "big picture."

Where are you coming up with this stuff? It seems like you are looking more for a "recipe" than scientific statements to support your claim.

Yes I am aware the 15 L/m is in your protocols as you did mention that in another thread. Again, can you support this with scientific evidence. I'm not judging whether you are right or wrong but I would like to read things to form my own opinion of the research for the subject matter that these statements are made from.

You are teaching a biochem class? College level? Your profile says you are working on a BA in math. You do contradict your earlier statement and it seems one would not have mistaken "taking" for "teaching.

I'll be sure to mention this to the biochem class I'm TAing this semester.

Your profile also says you want to get to med school. To be a physician one must also be a scientist. Making blanket opinionated statements and ignoring scientific literature will not do your patients any good. Your attitude is why a few ambulance services refuse to give up the MAST.

Did you bother to read any of the references I stated? Probably not.

As technology progresses we are able to study more concepts in medicine and how they affect the body. You need to open your mind to the world of science and medicine. At least when I get into a debate with JPINFV, Rid, MSDeltaFlt, Medic417, AKflightmedic, BossyCow, AJ, BLSboy, reaper and others, they put forth how they derived at their statements.

 

[DV_EMT]

By Technicallity,

O2 is considered not to be a drug "prescription wise". I've never worker in a pharmacy that has yet to dispense "O2". It is, however, considered to be a drug because it can be purchased by the public without a prescription much like tylenol or motrin.

so yes... it is considered a drug.

as for the pain portion of the discussion...

1. I learned that from a medic during my ride along.
2. I double checked it with both my EMT instructor (a medic and fire captain for 20 yrs) and the ICU/CCU pharmacist at my hospital
3. documentation... heres just one:

http://majidali.com/the_oxygen_view_of_pain.htm

 

[VentMedic]

3. documentation... heres just one:

http://majidali.com/the_oxygen_view_of_pain.htm

Excellent!

Actually, it is not just one reference. There are 41 references that went into the writing of that article.

References
1. Ali M. Oxygen and Aging. (Ist ed.) 2000. New York, Canary 21 Press. Aging Healthfully Book 2000.
2. Darnell J, Lodish H, Baltimore D. Molecular Cell Biology. 1990. New York. Scientific American Books. Distribted by WH Freeman and Company. pp 784-802.
3. Katz B. Nerve, Muscle, and Synapse. 2nd. ed. 1966. New York. McGraw-Hill.
4. Salerno, Evelyn, and Joyce S. Willens, eds. Pain Management Handbook: An Interdisciplinary Approach. St. Louis: Mosby, 1996.
5. Verbunt J, Seelen H, Vlaeyen J, et al. Disuse and deconditioning in chronic low back pain: concepts and hypotheses on contributing mechanisms. Eur J Pain 2003;7:9-21.
6. Krause JE, Takeda Y, Hershey AD. Structure, functions, and mechanisms of substance p receptor action. J Invest Dermatol. 1992;98:2S-7S.
7. Pernow B. Substance P. Pharmacol Rev. 1983;35:85-141.
8. Bolton TB, Clapp LH. Endothelial-dependent relaxant actions of carbachol and substance p in arterial smooth muscle. Br J Pharmacol. 1986;87:713-723.
9. Diz DI, Fantz DL, Benter IF, Bosch SM. Acute depressor actions of angiotensin II in the nucleus of the solitary tract are mediated by substance P. Am J Physiol. 1997;273:R28-R34.
10. Tagawa T, Mohri M, Tagawa H, Egashira K, Shimokawa H, Kuga T, Hirooka Y, Takea A. Role of nitric oxide in substance p-induced vasodilation differs between the coronary and forearm circulations in humans. J Cardiovasc Pharmacol. 1997;29:546 -553.
11. Naoko Kanda and Shinichi Watanabe . Substance P Enhances the Production of Interferon-induced Protein of 10 kDa by Human Keratinocytes in Synergy with Interferon- Journal of Investigative Dermatology 119, 1290-1297 (2002)
12. Kim DK, Oh EK, Summers BA, Prabhakar NR, Kumar GK. Release of substance P by low oxygen in the rabbit carotid body: evidence for the involvement of calcium channels. Brain Res. 2001 Feb 23;892(2):359-69.
13. Chen MJ, Chiang LY, Lai YL. Reactive oxygen species and substance P in monocrotaline-induced pulmonary hypertension. 1: Toxicol Appl Pharmacol. 2001;171:165-73.
14. Birklein F, Weber M, Neundorfer B. Increased skin lactate in complex regional pain syndrome: evidence for tissue hypoxia? Neurology. 2000;55:1213-5.
15. Leis S,WeberM, Isselmann A, SchmelzM, Birklein F. Substance-P-induced protein extravasation is bilaterally increased in complex regional pain syndrome. Exp Neurol 2003;183:197-204.
16. Ali Z, Raja S, Wesselmann U, et al. Intradermal injection of norepinephrine evokes pain in patients with sympathetically maintained pain. Pain 2000;88:161-8.
17. Koban M, Leis S, Schultze-Mosgau S, et al. Tissue hypoxia in complex regional pain syndrome. Pain 2003;104:149-57.
18. Zollinger P, Tuinebreijer W, Kreis R, et al. Effect of vitamin C on frequency of reflex sympathetic dystrophy in wrist fractures: a randomised trial. Lancet 1999;354:2025-8.
19. Perez R, Zuurmond W, Bezemer P, et al. The treatment of complex regional pain syndrome type I with free radical scavengers: a randomized controlled study. Pain 2003;102:297-307.
20. Noguchi K et al: Substance P induced by peripheral nerve injury in primary afferent sensory neurons and its effect on dorsal column nucleus neurons. J Neurosci. 1995;15:7633.
21. Milan P Stojanovic M. Stimulation Methods for Neuropathic Pain Contro. Current Pain and Headache Reports 2001, 5:130-137. // MGH Pain Center Department of Anesthesia and Critical Care, 15 Parkman Street, Massachusetts General Hospital, Boston, MA, 02114, USA // Current Pain and Headache Reports 2001, 5:130-137.
22. Ochoa J, Verdugo R. Mechanisms of neuropathic pain: nerve, brain, and psyche: perhaps the dorsal horn but not the sympathetic system. Clin Auton Res 2001;11:335-9.
23. Sicuteri F, Fanciullacci M, Nicolodi M, et al. Substance P theory: a unique focus on the painful and painless phenomena of cluster headache. Headache 1990;30:69-79.
24. Lynn B. Capsaicin. Actions on nociceptive C-fibers and therapeutic potential. Pain 1990;41:61-9.
25. DiSabato F, Giacovazzo M, Cristalli G, et al. Effect of hyperbaric oxygen on the immunoreactivity to substance P in the nasal mucosa of cluster headache patients. Headache 1996;36:221-3.
26. A. C. Brooks*,1, C. J. Whelan1 and W. M. Purcell2. Reactive oxygen species generation and histamine release by activated mast cells: modulation by nitric oxide synthase inhibition. British Journal of Pharmacology 128:585-590 (1999)
27. Fusco BM, Fiore G, Gallo F, et al. "Capsaicin-sensitive" sensory neurons in cluster headache: pathophysiological aspects and therapeutic indication. Headache 1994;34:132-7.
28. Ali M. Nature's Preoccupation With Complementarity and Contrariety, The Principles and Practice of Integrative Medicine Volume II. 2001. Washington, D.C. Capital University Press (in collaboration with Canary 21 Press, New York). www.cuim.edu & www.Canary21press.com)
29. Baynes J, Dominiczak MH. Medical Biochemistry. 1999. New York. Mosby. pp31-39.
30. Pascual J, Peralta G, Sanchez U. Preventive effects of hyperbaric oxygen in cluster headache. Headache 1995;35:260-1.
31. Mendizabal JE, Umana E, Zweifler RM. Cluster Headache: Horton's Cephalalgia Revisited. South Med J 1998;91:606-17 [review].
32. Ali M. The Cortical Monkey and Healing. 1991. Bloomfield, New Jersey. Life Span Books 1991.
33. Ali M. Miracles, and the Bite of the Gray Dog, 1997. Denville, New Jersey, Life Span Books.
34. Fogan L. Treatment of cluster headache. A double-blind comparison of oxygen v air inhalation. Arch Neurol 1985;43:362-3.
35. Kudrow L. Response of cluster headache attacks to oxygen inhalation. Headache 1981;21:1-4.
36. H eterocephalus glaber. www.sciencedaily.com/releases/2003/11/031117073925.htm
37. DiSabato F, Fusco BM, Pelaia P, Giacovazzo M. Hyperbaric oxygen therapy in cluster headache. Pain 1993;52:243-5.
38 Ali M: Fibromyalgia: an oxidative-dysoxygenative disorder (ODD). J Integrative Medicine 1999; 3:17-37.
39. Ali M: Darwin, fatigue, and fibromyalgia. J Integrative Medicine 1999;3:5-10.
40. Ali M: ODD trigger points in fibromyalgia: pathogenesis, diagnosis, and resolution J Integrative Med 1999; 3:38-47.
41. Stanton-Hicks M, Janig W, Hassenbusch S, et al. Reflex sympathetic dystrophy: changing concepts and taxonomy. Pain. 1995;63:127-33. Also: Drummond P D. Involvement of the sympathetic nervous system in complex regional pain syndrome. ijl.sagepub.com/cgi//reprint.

 

[DV_EMT]

I was hoping that you'd catch that

 

[syd]

Not to get off the subject of O2 and pain, but, can a EMT-Basic even get certed for ACLS? I heard that you can go through the class and learn the stuff but can't a cert for it... I'm confused... maybe I need O2... does it help with confusion???

 

[rmellish]

Not to get off the subject of O2 and pain, but, can a EMT-Basic even get certed for ACLS? I heard that you can go through the class and learn the stuff but can't a cert for it... I'm confused... maybe I need O2... does it help with confusion???

If you pass the course then I'm fairly sure you can get your ACLS course completion card. This will not change your scope of practice as a basic.

 

[reaper]

Not to get off the subject of O2 and pain, but, can a EMT-Basic even get certed for ACLS? I heard that you can go through the class and learn the stuff but can't a cert for it... I'm confused... maybe I need O2... does it help with confusion???

They do not certifiy you for anything. They give you a completion card. No, they will not give an EMT a card, unless you are in Medic school at the time of the class.

 

[NorCalMedic]

They do not certifiy you for anything. They give you a completion card. No, they will not give an EMT a card, unless you are in Medic school at the time of the class.

This is true. I teach this class and some proavtive EMT's like to know that sort of stuff. Unfortuneately they will not give you a card, but they may give you the CE's for taking the class which could be equally as useful!

 

[syd]

This is true. I teach this class and some proavtive EMT's like to know that sort of stuff. Unfortuneately they will not give you a card, but they may give you the CE's for taking the class which could be equally as useful!

They won't give you which card? The ACLS or the EMT?

 

[NorCalMedic]

They won't give you which card? The ACLS or the EMT?

They will not provide you with an ACLS card if you are an EMT taking the ACLS class.

 

[Jon]

OK - My understanding of ACLS was that you needed to be a higher-level medical provider to be allowed to take the class... is that correct?

 

[8jimi8]

no, i took ACLS and PALS as a nursing student and was given the certification card.

 

[VentMedic]

no, i took ACLS and PALS as a nursing student and was given the certification card.

True. RT and Paramedic students will also be given a card as it is usually a requirement to complete their programs. It may be required for these professionals (to be) and not for the EMT-B.