"The Rhode Island protocols are terrible," my partner tells our patient, a nurse.
"Why?" I ask, "I think the BLS protocols are great."
In Rhode Island, EMT-Bs have a wide scope of practice that allows them to deal with a number of situations without the need for ALS.
"Well, for example, Albuterol is in the CHF protocols. Albuterol will kill someone in CHF. When I showed that to my medic instructor in Massachusetts, he just laughed."
I roll my eyes. "I've had this debate before," I tell him. "Why do you think that Albuterol kills people in CHF?"
"The wheezing you hear in CHF is from compensatory bronchoconstriction. It's the body's defense mechanism, and it prevents edema from filling up the lungs. Albuterol opens up the airway and increases the negative pressure in the lungs that draws in each breath, and also helps draw fluid into the alveoli."
It's a new one. In the past I've been told that albuterol opens up the upper airways, directly creating more space for fluid to fill the lungs, or that albuterol is bad because it allows fluid to return to circulation before the fluid overload problem has been resolved. Either way, I've been laughed at for suggesting that albuterol might not really be that bad, and yet I've never been given a satisfactory mechanism through which it kills all the victims of the terrible Rhode Island congestive heart failure protocol.
The first thing I did was look up the contraindications to albuterol through epocrates on my iphone. This is what I found:
While neither pulmonary edema nor CHF is listed as a contraindication or caution to albuterol administration, many common CHF comorbidities–ischemic heart disease, hypertension, arrhythmia, diabetes, and old age- are. Nonetheless, I point this out to my partner:
"If albuterol were really so terrible for CHFers, don't you think CHF or pulmonary edema would be listed as a contraindication in the drug insert?" I ask him.
"I don't go by drug inserts," he tells me. I wonder what he does go by.
Well, after some debate, and being told that I've forgotten my anatomy and physiology, I'm still not satisfied, so when I go home I surf over to pubmed to see what I can find. I type in "albuterol" and "congestive heart failure" and am happy to see the first result:
Maak A, Tabas J, and McClintock D. Should Acute Treatment with Inhaled Beta Agonists be Withheld from Patients with Dyspnea Who May Have Heart Failure? Journal of Emergency Medicine. 2008 (published online before print)
This paper is a meta-analysis of 24 different studies on the effects of beta-agonists, including albuterol, in patients with heart failure. Here are some interesting points:
- Many patients with chronic heart failure who do not have COPD as a comorbidity still have an airway obstruction problem–"cardiac asthma"– that results from CHF directly. When bronchial vessels become congested, edema of the airway wall occurs, much as pulmonary edema occurs when pulmonary vessels become backed up. The plasma that causes the edema also brings with it paracrine cell-signaling molecules that are bronchoconstrictors, and further cause upper airway swelling.
- We know that albuterol decreases bronchial edema, but in animal and human trials, it has also been shown to increase fluid clearance from the alveoli themselves. In one sheep study, nebulized salmeterol, another beta-2 agonist, decreased pulmonary edema by 60%.
- 20 human studies demonstrated a 13-51% reduction in systemic vascular resistance after administration of beta-2 agonists in heart failure patients.
- While the beta-1 effects of albuterol might be concerning when treating a patient in heart failure or with a suspected MI, one study showed that 31 patients suffering from MI and cardiogenic shock improved hemodynamically when administered albuterol, and none developed worsening ischemia. Two other studies found similar results in patients with left sided failure. In other words, the benefit derived from decreasing cardiac workload indirectly by decreasing respiratory effort outweighs any increase in workload caused by increased heart rate or contractile force.
- Chronically administered inhaled beta-2 agonists have been associated with increases in mortality, incidence of dysrhythmias, and hospitalization for CHF in heart failure patients. Despite the trend, the causal link is unestablished.
- The authors were unconcerned with the possibility of pulmonary edema when acutely administering beta-2 agonists to CHF patients. They were more concerned with the possibility of dysrhythmia secondary to beta-2 agonists' induction of hypokalemia, or low potassium. However, no link was found between inhaled beta-2 agonist use and an increase in incidence of dysrhythmia in heart failure patients.
I'm not saying that my next CHF patient is going to see me walk into the room with an albuterol bullet in hand; they won't. But, if after a nitro or two and some Lasix, I hear wheezes in the upper fields, I certainly won't worry about albuterol causing a biblical-lung-flood. And if I'm debating the cause of a patient's dyspnea, it's good to know that albuterol may help, even if left ventricular failure is to blame.
I was going to print out a copy of this paper to show to my partner, but then I remembered what he told me– "I can get a study to say anything." Good thing he's got all those anecdotes and that in-depth understanding of A&P to rely on.
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17 comments:
Great post.
I think this is really a perfect example of the issues with pre-hospital education. Because EMS educators don't need any higher education or a formal science background, a poor grasp of physiology and pathophysiology is simply passed on to the next generation. Additionally, because of the generally low standards of education of providers (I mean, they even let ME in haha), we find these myths lasting for years before being dispelled. 10 years ago, the emergency medicine world knew that MAST trousers didn't work, yet they still were popular and in use a few years ago. Until pre-hospital care really becomes an evidence based medicine, inaccuracy, myths and falsities will continue to plague our profession.
To comment more specifically on this topic, I think the future of the treatment of these patients most likely lies in treatment that are mechanical in nature rather than pharmacological, such as pre-hospital CPAP. Research shows PEEP being extremely effective in COPD/Asthma management and I think we can expect it to find its way into protocol in the not-so-distant future.
In the end, it's posts like this which can ultimately raise provider awareness and help dispel inaccuracies.
Are you planning on featuring more discussions covering patient care and treatments in the future? I dig it
-MedicTrunkMonkey®
Hmm...
I want there to be content for non-medical/EMS people, but I did like writing this. I'll try to keep it varied. Stay tuned for Para-myth #231: The NPA goes in the brain.
Thanks for the comment, dude.
-Dan
I believe the understanding of the arguement, if I recall correctly, was that Albuerol would be a poor choice as a "first line medication treatment for a CHFer." This being the RI protocals RECOMMENDATION for a first line treatment. I think that after our reltive debate, we had mutually agreed that Albuterol would be a good drug to use to clear up bronchioconstriction AFTER aspirin, nitro, and positive pressure ventilation had been established, or at least High flow O2. I, personally, were I an ALS provider, would only give the albuterol after I had vasodialated the veins to give the fluid a place to go to; followed by PPV to push the remaining fluid out. The ASA would be to prevent against clotting hat could result in an MI or a CVA down the road. Albutrol would be after all of this to helpease the patient in thier breathing.
Of course every EMT and healthcare provider will vary at some length as to how care can be provided, but in the long run, would hope that the end result would be that we help our patients, and, hopefully, have done our jobs and save lives.
I hope that, in the future, we may have other intelligent conversations and debates to further our knowledge. I think the moral of this story should REALLY BE that we both went home and examined beta 2 agonists and somewhat adavnced out knowledge on this class of drugs, wouldn't you agree??
-The "Partner" from WFD
"Our duty is done. The rest is in God's hands"
Hello- I am a paramedic with 20 years of field experience and advanced college education and as many years of experience in teaching ACLS and other EMS courses. I'm not saying giving albuterol is going to instantly kill a CHF patient. However, I am taken by your 'first do no harm' logo on your page here. The fact that the list of cautions for albuterol includes elderly, hypertension, heart disease, hypokalemia and other conditions that can be comorbid with CHF is reason enough to knock albuterol to the very bottom of the list of potential treatments for CHF, if not off the list entirely. I believe new medics... all medics... Should STRONGLY resist the urge to administer albuterol to a CHF patient. Do a proper H&P, including medication history. Example: I just finished a call this evening for an 89yo f short of breath. The vol fire dept medic was first to arrive and had a neb ready, but thankfully did not have the albuterol with him. She did sound wheezy without even using a steth, but he completely failed to get a medication hx... NO respiratory meds, but was on lasix, isosorbide and lisinopril, among others. Upon exam, I also detected sales in the bases. I declined the albuterol and started ntg q5min and also gave lasix 40mg IV. Unfortunately, we do not have positive pressure in our protocols yet. Within 15 min of the first ntg her wheezing was gone and all she had were minor crackles in the bases at the hospital. Think about what's happening in CHF. Do you really think it's a good idea to increase a patient's heart rate with a beta agonist and potentially increase myocardial oxygen demand in a patient who may very well have some acute cardiac ischemia? If you pay strict attention to treating the CHF properly, you will remove the irritant (fluid) that is causing the reflex bronchoconstriction that is causing the 'wheezing' or cardiac asthma. Albuterol should not be a first line by any means, and I would say not at all unless they have significant respiratory comorbidity and only after the CHF has been addressed with appropriate treatment for CHF.
I hate to bring a long dead post back to life, but find I must. Frankly, I think your partner is more correct than you in this instance.
While Albuterol is very unlikely to do harm to a CHF patient, there is scant evidence that it does much good. The theory is that it might help to mobilize fluid in the bronchial tree, but the study evidence isn't particularly strong. There is some risk of increasing tachycardia and BP in patients with CHF and that could well add to the cardiac load on patients that are already compromised.
Even the studies you cite aren't particularly clear cut and if your goal is to clear fluid from the lungs (which it is), high doses of SL NTG (although IV NTG would be better) combined with CPAP are far more effective. Remember, we're not draining the lungs, we're creating conditions where the lungs can drain themselves. Lower diastolic filling pressure, which CPAP and NTG do, is the better mechanism.
CPAP is far better than Albuterol without the downside. The only constraints for CPAP are hypotension and patient tolerance of the mask.
In fact, given the opportunity, I'd rather have BLS personnel use CPAP than Albuterol for CHF patients.
Does the pulmonary congestion in CHF act as a surrogate for bronchoconstriction or is there actual bronchoconstriction? Good question and I don't know the answer. What I can tell you is that in CHF there is no prolongation of expiration as there is in reactive airway disease. Nor is there any evidence of CO2 retention, as with RAD.
So, while para-myth #472 isn't true, it's not clear that your position is not para-myth #473. Especially when better treatment modalities exist.
My mother (74 yes) was in the ER and had high levels of potassium. She was a dialysis patient with a history well known to this hospital, of HOCM (this is what the hospitality said). When the respitory therapist came in to give her two nebs of albuteral I told her that my mom's primary Dr said she would never give her albuteral because of her heart issues and the response was that they do a lot of things in the ER that your primary wouldn't do. So I dropped the issue. Not an hour later my mom had a massive heart attack. A hospialist told me that albuteral was the quickest and cheapest way to lower potassium. Always a comfort that so much thought had been put into her care. Quick and cheap, I will not forget that description.
Since there is no evidence of CO2 retention- don't forget the other component in respiration during exhalation- h20. Ng with albuterol would help. PEEP is a plus if Ng on board.
I think some protocols carried zoponex for peds because of less beta 1- it may have been pulled..maybe check into others.
I have had trouble breathing for years and my family physician gave me albuterol and it worked so I always assumed I had asthma. My pulmonary doctor later told me my lungs look great. I'm 42 and just found out I have lowered ejection fraction heart failure in my home town on the east coast. When I returned home out west in a little retirement town the heart doctor looked at me and pretty much laughed at my diagnosis saying I was too young and never tested me. I still have serious difficulty breathing upon exertion and I turn right to my albuterol. As always I get instant relief. My heart does have irregular beats but I would faint without albuterol. I know I'm not elderly yet and maybe it would kill me at a later age with heart failure. I found this page by trying to research if albuterol works does that mean I am definitely having asthma? This is good to know that it helps one breath with heart failure when your gasping for air and couldn't even walk 50 ft to your car to get to a hospital. Thank you so much for writing this page. Please please pleas any feedback would be GREAT!
Hate to say but every single one of yall are wrong on the this subject except for the poster that posted about this , not all chf patients are the same and are very different .
It's more important to treat the patient and his/her symptoms and forget about preconceived protocols & algorithms. When discussing CHF pts so many providers fail to grasp the many forces at work against the patient, the these pts exist in such a chronic state of compensation, that when they are pushed ever so slightly passed their body's comfort level, the acuity of of their chronicity is tantamount to the struggle between David and Goliath. We're just not attempting to fixed their respiratory distress, or exertions dyspnea, or bronchial wheezing, underneath it all, we are battling months, maybe years of exacerbated and prolonged humeral & neurohumeral compensatory mechanisms that entirely out of control, so much in fact, that these once hemodynamically protective responses are now responsible for increased cardiac workload, increased myocardial oxygen demand and usage, worsening ventricular performance, life-threatening electrolyte imbalances, chronic imposed states of hypovolemia, hypovolemic shock, and unmanageable changes in that patient's general protein levels, albumin levels, colloid osmotic levels, plasma volume, interstitial fluid levels, hydrostatic pressure levels, and extracellular fluid levels. Not to mention the influences from Starling forces, including venous capillary pressures, etc. Heck, the body interprets, and essentially exists in a chronic state of SHOCK. So, it goes without saying it's as simple to say 'yea' or 'nae' for which treatments you should implement for your CHF'er. Great discussion. Posters made many great points about A&P, pharmacokinetics, treatment trends, and, of course, individual nuances among different CHF patients. "Look for the zebra, but don't forget the horse!"
Above article is really helpful for taking about heart attack patients to help with care of them.Thanks for sharing valuable information about heart attack patients.
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