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I found this in the drug insert for the adenosine that we use: "Adenosine administration by inhalation has been reported to cause bronchoconstriction in asthmatic patients, presumably due to mast cell degranulation and histamine release. These effects have not been observed in normal subjects. Adenocard has been administered to a limited number of patients with asthma and mild to moderate exacerbation of their symptoms has been reported. REspiratory compromise has occured during adenosine infusion in patients with COPD. Adenocard should be used with caution in patients with obstructive lung disease not associated with bronchoconstriction (i.e. emphysema, bronchitis, ect.) and should be avoided in patients with bronchoconstriction or bronchospasm (e.g. asthma). Adenocard should be discontinued in any patient who develops severe respiratory difficulties."

From what the latest AHA guidelines say, only ASA has been proven to reduce mortality for patients suffering MI's. Is it really true that there are no studies that have proven the effectiveness of nitro? Are we just using just because that's what we've always done and because there seems to be an explanation for how it can work in reducing the size of an infarct?

Do you guys clearly see delta waves here? I'm not too familiar with them---I understand that they are complexes with slurred or notched R waves.

Although I"m only 5 minutes from the hospital, I would cardiovert her again. Asking the hospital what to do may be bad advice because this is not a situation where you have someone in a stable wide-complex tachycardia of unknown type. If I really knew that it was WPW, then I would cardiovert her again. From what I've read about WPW, it is much more dangerous than other causes of SVT and must be treated more aggressively because even in a young person it can quickly progress into ventricular fibrillation.

Ok, thanks Ridryder 911. I'll have to check into that.

If you like that blog, you should check out Peter Canning's. I've read a bunch of EMS memoirs, but his two books are the best I've found. http://petercanning.org/index.htm

AZCEP wrote: "Abdominal thrusts for the conscious FBAO patient are being de-emphasized anyway. For most, they are ineffective and unable to remove the obstruction." Could you elaborate? I haven't heard this before. I've never had do give abdominal thrust before, but I've heard many stories of them being effective.

Here is a case study from a site for med students. The patient was given albuterol, after which her HR jumped from 115 to 189. Note that they say that adenosine is contraindicated with bronchospasm. What do you guys think? http://clinicalcases.blogspot.com/2004/01/...ol-what-is.html ---------------- SVT - HR 189 bpm after Albuterol, What is TSH? Author: V. Dimov, M.D., Cleveland Clinic Reviewer: A. Aneja, M.D., Cleveland Clinic 70 yo AAF is admitted to the hospital with CC: SOB x 2-3 days. PMH: COPD on home O2, multiple episodes of CP, catheterization showed normal coronaries 1 year ago (0% stenosis), EF 65%, HTN. SOB is typical of her COPD exacerbations. The patient is a member of the so called "50-50 club", which means that both her PaCO2 and PaO2 are in the range of 50 mm Hg. She is visibly SOB and not able to talk with full sentences. On physical exam she is using accessory muscles, tachycardic at 125 bpm, and not moving much air. She has never been intubated before. SpO2 is 94% on 3L. Her home O2 is 2L/min. After one aerosol treatment with Albuterol, her HR increases to 189 bpm, BP is 150/90. The monitor shows a narrow complex tachycardia and she is fully AAO x 3. What is going on? Narrow complex tachycardia in response to Albuterol? R/O ischemia - but the coronaries are normal? What to do? Follow the ACLS guidelines. The carotid sinus massage failed to slow down the HR. Adenosine and Lopressor are contraindicated b/o bronchospasm. Try Cardizem? What happened? Cardizem 10 mg IV over 2 min brought HR down to 115 over 7 minutes. The patient felt better. Her aerosol Tx was switched to Xopenex and Atrovent. Solu-Medrol 40 mg IV q 6 hr was started. TSH is <0.05 style="font-weight: bold;">Final diagnosis: Narrow complex tachycardia due to hyperthyroidism and Albuterol. Ischemia was ruled out. Spiral CT ruled out PE (probably not needed - PaO2 was at baseline) What did we learn from this case? Always order TSH in the tachycardia work-up. Cardizem works and it is usually safe. Adenosine and beta-blockers are CI in acute bronchospasm. Created: 04/2006 Updated: 03/05/2007

What an interesting topic. This is why I love this site!

Dustdevil, What do civilian medics do in Iraq? Do they work at military clinics? Are you in the military? What exactly do you do? I'm sure people on this forum would love to hear your stories.

No, I'm not still in school. I use luer locks connected to the IV catheter. I then connect the IV line or med bag to that luer lock. So, if I were to connect the med bag to the luer lock, I could easily disconnect it (and attach the IV line) if there was any problem. It just seems like this would be faster than having to set up a piggyback.

I've worked for AMR for five years. They suck. They only care about increasing their profits, not about their employees or patients. You guys should do everything you can to keep AMR out.

I guess I'm partially answering my own question, but I remember now that Torsades sometimes can't be synched. What about a very fast A Fib?

Why do we piggyback meds like dopamine? Why not just connect the bag with the dopamine directly to the IV catheter?

In what circumstances might it not be possible to synch before cardioverting? Very rapid AF? In this situation, would it be okay to instead defib at a high energy (i.e., 200 J)?

Thanks, Scatrat!

Sorry, I should have been more clear. What I mean is, how do you change the set up/configuration. For example, if you always want the monitor to show leads I, II, and capnography, or if you want to always have the pacer be in demand mode, or whatever.

I was thinking that for a patient in a stable, wide-complex tachycardia, the lidocaine can have a quicker effect since you can give it IVP. Am I wrong about this?

I'm trying to understand the pathophysiology behind uncontrolled AF with a very fast rate (over 160). I understand that for other SVT's, the cause is either an accessory condution pathway (as in WPW) or a re-entry mechanism in the area of the AV node. So how is it that you get AF with very fast rates? Is the AV node defective in not being able to block all these impulses, or is there also some sort of re-entry mechanism going on?

How do you program LP 12's?

When a patient is in stable VT and you have the choice of giving amiodarone or lidocaine, wouldn't it be better to give lidocaine since it won't take so long to set up and administer as the amiodarone drip? In the area where I work we are usually just 5 to 10 minutes from the hospital.

If a patient is on beta blockers, how effective will albuterol be?

this guy has two things going on, respiratory distress and a dangerously fast heart rate. the heart rate is not just a response to the respiratory distress (like a sinus tach, of, say, 130, might be); rather, it's a problem in itself. there's no question that you're going to do everything you can to treat the respiratory problem. the question that the author asks is do you also treat the uncontrolled AF. he is saying no, you shouldn't. i think his case is well argued, but it just seems reasonable to me that you would try to cardiovert. if he's hypoxic and at the same time his heart is beating that quickly, it seems like it's only a matter of time before his oxygen-starved myocardium will go into V-fib.

of course you'd also treat the respiratory distress, but why not do both at the same time?

I recently read an article in JEMS by James F. Goss about cardioversion of atrial fibrillation with a rapid ventricular response rate being contraindicated for a severe underlying pulmonary disorder. I'm not sure if I agree. What do you guys think? Check out the article below (all spelling mistakes are mine, not the author's, as I had to retype it since I could not find a link!) Complex Cardioversion By James F. Goss You’re dispatched to the residence of an elderly male with difficulty breathing. On arrival, you find a 74-y/o male in severe respiratory distress. He has altered mental status and appears to need to sit up to breath. His wife reports he has a two-day history of progressive dyspnea much worse than his baseline, as well as a history of emphysema, atrial fibrillation (AF), CHF, and continued smoking. The patient is cachectic, appears wasted, and has dry, flaky skin except around his lips, which are blue. Your assessment reveals significant suprasternal and intercostal retractions, absent breath sounds bilaterally, and use of accessory muscles. Vitals: BP 92/48; pulse thready and unable to count at fast rate; RR 44. Also observed is 4+ pitting pedal edema, extending to mid-calf, and mild abdominal distention. A cardiac monitor reveals an unusually high tachyarrhythmia with an irregular rate of around 220. (Note: rates are usually significantly lower.) Due to the increased heart rate, it’s difficult to discern the underlying rhythm. Your partner, also a paramedic, insists on attempting synchronized cardioversion per local protocol for symptomatic tachyarrhythmia with rates greater than 150. You think the respiratory compromise should be treated first, and you contact your base station. The base station agrees that cardioversion isn’t the best approach in this case and directs code 3 transport with respiratory care, including high-flow 02 and albuterol. Although the monitor reveals a tachyarrhythmia with a ventricular rate of 220, this isn’t the primary problem. The tachyarrhythmia is secondary to the severe exacerbation of the patient’s emphysema and the attendant hypoxemia and myocardial ischemia. This patient has a history of COPD and chronic AF, as well as CHF....[i’m leaving out some of the authors explanations of these diseases.]……and increased symptomatic tone usually worsens that condition, as do the hypoxia and increased anxiety and stress of respiratory decompensation. Exacerbation of your patient’s respiratory condition, along with hypoxemia and hypercapnia, contribute to increased sympathetic tone and subsequent increase in heart rate. AF can be accompanied by ventricular response rates up to 300. Most cases of AF are chronic and shouldn’t be cardioverted due to the high risk of post-conversion embolic stroke along with the fact that chronic AF will reoccur within a very short time. So would cardioversion by the best choice for a patient with poor air movement and hypoxemia? After all, when we hit the “reset button” on the heart through cardioversion, the cardiac cells require oxygen to restart. Thus, cardioversion of AF with a rapid ventricular response rate is contraindicated for a severe underlying pulmonary disorder. Treatment to improve oxygenation should be initiated immediately. Improving ventilation and oxygenation will likely result in a decrease in sympathetic tone and heart rate. Although CPAP would be a better choice, IV diltiazem or verapamil may be indicated to slow the heart rate, improve ventricular filling, and decrease myocardial oxygen demand. During transport, the patient’s respiratory status improved mildly as reflected by an increase in audible air movement on auscultation of the lungs, improved saturation, and a mildly decreased heart rate. Despite these changes, the patient remains in severe distress on ED arrival. In the Ed, his heart rate is slowly reduced and his status improves, and that patient is later transferred to the ICU.