Albuterol/CHF

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Permalink Reply by TheCannulator on October 6, 2009 at 1:12am

We recently improved our guidelines to reflect this with APO/CCF. To consider not treating with salbutamol without considering cardiogenic causes. It's more about appreciating that the pulmonary fluid may be causing the bronchospasm, so treating the failure and improving ventilation may be more useful than just the resultant wheeze.
I'll see if there is anything that I can dig up.

Be suspicious of new bronchospasm in the elderly is worthwhile.

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Permalink Reply by Tom Bouthillet on October 6, 2009 at 8:37am

Maybe it can help for a small subset of patients experiencing so-called "cardiac asthma" who are moving enough air to get the albuterol far enough into the bronchial tree where it helps, but 99% of the time when I see paramedics giving a breathing treatment to a CHF patient it's because they don't realize that they're dealing with acute pulmonary edema. If they did realize it, they'd be giving NTG. If the patient has a cardiac history, is hypertensive, short of breath, has adventitious breath sounds (especially basilar rales), and is normothermic, I treat it as pulmonary edema (even if it's a little bit wheezy). On the rare occasion that I give albuterol, I use both oxygen trees and place the patient on a NC @ 4 LPM along with the handheld nebulizer, since a tired CHFer spends a lot of time with the inhaler away from the face. My service is late into the CPAP game (we're implementing it in the next 30 days) but it seems to me that NTG and CPAP is the way to go. It should also go without saying that new onset pumonary edema should be treated as a possible ACS until proven otherwise.

Tom

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Permalink Reply by Neil White on October 6, 2009 at 10:52am

From a UK spin, our protocol suggests;

giving it more on a basis of diagnosis uncertainty and possibility of misdiagnosis. It is part of the management protocol to avoid depriving copd/asthma patients of vital brochodialators.

Don't know if that helps any?

Attachments:

• pulmonary_oedema_2006.pdf, 130 KB

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Permalink Reply by Scott RB on October 6, 2009 at 11:14am

Albuterol for CHF is pretty controversial where I work. Many medics (myself included) have seen patients deteriorate after a neb treatment in cases where the initial presentation was ambiguous. There are two hypotheses that get thrown around: 1. By causing the bronchioles to expand, fluid is forced from the interstitial space into the alveolar space resulting in flash pulmonary edema; or 2. the albuterol opens them up enough to appreciate the rales/crackles. Some medics I work with seem to think that giving albuterol is VERY BAD and should NOT EVER be done. I've tried to look into "cardiac asthma" and its causes and treatment approach (e.g. just treat the CHF w/ standard treatment, or both standard treatment and albuterol). Interestingly, I have found quite a few studies where CHF patients were given methacholine (or similar) challenges and evaluated for bronchoconstriction, and these have found that many CHF patients (and also those with mitral valve stenosis) have hyperreactive airways despite absence of history of asthma and absence of COPD. This leads me to believe that for a chronic CHF patient with what is believed to be a "cardiac wheeze" may benefit from a breathing treatment with albuterol.

There was a study (Ann Emerg Med. 2008 Jan;51(1):25-34.) that correlated use of albuterol in acutely decompensated CHF (without history of COPD) with worse outcomes, however the study was retrospective and was unable to determine causality - in other words, were the patients that received albuterol generally more sick or was their condition worsened by albuterol? No one knows.

Some abstracts:

Jpn Circ J. 1996 Dec;60(12):933-9.Click here to read Links
Relationship between bronchial hyperreactivity and symptoms of cardiac asthma in patients with non-valvular left ventricular failure.
Nishimura Y, Maeda H, Hashimoto A, Tanaka K, Yokoyama M.

First Department of Internal Medicine, Kobe University School of Medicine, Japan.

To determine whether a relationship exists between bronchial hyperreactivity and cardiac asthma, which is commonly observed in patients with left heart failure, a methacholine inhalation test was performed in 15 patients with stable left ventricular failure (LVF) and 10 normal subjects. The subjects were divided into 3 groups based on symptoms of nocturnal coughing and/or wheezing in acute exacerbation of LVF. Group A consisted of 8 patients with nocturnal coughing and/or wheezing. Group B consisted of 7 patients without such symptoms, and Group C consisted of the 10 age-matched normal controls. Eleven of the 15 patients with LVF showed a significant increase in respiratory resistance in the methacholine inhalation test, as opposed to none of the normal subjects. The median cumulative dose which produced a 35% decrease in respiratory conductance (PD35Grs) was significantly lower in Group A than in Group B (1.45 log units and 1.90 log units, respectively, p < 0.05). The results of pulmonary function tests were not significantly different between Groups A and B. The minimum cumulative dose required to initiate a decrease in respiratory conductance from the baseline, as an index of bronchial sensitivity to methacholine, was significantly correlated with DLCO/VA (r = 0.710, p < 0.01). We conclude that bronchial hyperreactivity is responsible for cardiac asthma and that it might be related to pulmonary interstitial changes in stable patients with non-valvular LVF.

N Engl J Med. 1989 May 18;320(20):1317-22.Links

Comment in:
N Engl J Med. 1989 Dec 21;321(25):1756-8.

Bronchial hyperresponsiveness to methacholine in patients with impaired left ventricular function.
Cabanes LR, Weber SN, Matran R, Regnard J, Richard MO, Degeorges ME, Lockhart A.

Department of Physiology, Université René Descartes, Hôpital Cochin, Paris, France.

To elucidate the pathogenesis of bronchospasm in congestive heart failure, we studied 23 patients with chronic impairment of left ventricular function due to coronary artery disease or dilated cardiomyopathy. In 21 of them we found marked bronchial hyperresponsiveness to methacholine. The mean dose (+/- SD) of methacholine that elicited a 20 percent decrease in the forced expiratory volume in one second (FEV1) was 421 +/- 298 micrograms, nearly the same as in patients with symptomatic asthma. In contrast, there was no bronchial response to methacholine in 9 of 10 patients who had coronary artery disease but normal left ventricular function. Administration of the bronchodilator albuterol led to a partial (43 percent) reversal of the methacholine-induced bronchial obstruction. In 12 patients, pretreatment with the alpha-adrenergic agonist methoxamine (10 mg by inhalation), a potent vasoconstrictor, fully prevented the methacholine-induced decrease in FEV1. The protective effect of methoxamine was blocked by the alpha-adrenergic antagonist phentolamine in all six patients who received this agent. We conclude that bronchial hyperresponsiveness to cholinergic agonists is frequent in patients with impaired left ventricular function and may contribute to the wheezy dyspnea commonly observed in such patients. The bronchoconstriction may be mediated at least in part by dilatation of the bronchial vessels.

BMC Cardiovasc Disord. 2007 May 14;7:16.Click here to read Click here to read Links
Cardiac asthma in elderly patients: incidence, clinical presentation and outcome.
Jorge S, Becquemin MH, Delerme S, Bennaceur M, Isnard R, Achkar R, Riou B, Boddaert J, Ray P.

Department of Emergency Medicine and Surgery, Centre Hospitalo-Universitaire (CHU) Pitié-Salpêtrière, Assistance-Publique Hôpitaux de Paris, Paris, Université Pierre et Marie Curie-Paris 6, France. stephanejorge@voila.fr

BACKGROUND: Cardiac asthma is common, but has been poorly investigated. The objective was to compare the characteristics and outcome of cardiac asthma with that of classical congestive heart failure (CHF) in elderly patients. METHODS: Prospective study in an 1,800-bed teaching hospital. RESULTS: Two hundred and twelve consecutive patients aged > or = 65 years presenting with dyspnea due to CHF (mean age of 82 +/- 8 years) were included. Findings of cardiac echocardiography and natriuretic peptides levels were used to confirm CHF. Cardiac asthma patients were defined as a patient with CHF and wheezing reported by attending physician upon admission to the emergency department. The CHF group (n = 137) and the cardiac asthma group (n = 75), differed for tobacco use (34% vs. 59%, p < 0.05), history of chronic obstructive pulmonary disease (16% vs. 47%, p < 0.05), peripheral arterial disease (10% vs. 24%, p < 0.05). Patients with cardiac asthma had a significantly lower pH (7.38 +/- 0.08 vs. 7.43 +/- 0.06, p < 0.05), and a higher PaCO2 (47 +/- 15 vs. 41 +/- 11 mmHg, p < 0.05) at admission. In the cardiac asthma group, patients had greater distal airway obstruction: forced expiratory volume in 1 second of 1.09 vs. 1.33 Liter (p < 0.05), and a forced expiratory flow at 25% to 75% of vital capacity of 0.76 vs. 0.99 Liter (p < 0.05). The in-hospital (23% vs. 19%) and one year mortality (48% vs. 43%) rates were similar. CONCLUSION: Patients with cardiac asthma represented one third of CHF in elderly patients. They were more hypercapnic and experienced more distal airway obstruction. However, outcomes were similar.

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Permalink Reply by dr-exmedic on October 6, 2009 at 9:30pm

Scott RB said:

There was a study (Ann Emerg Med. 2008 Jan;51(1):25-34.) that correlated use of albuterol in acutely decompensated CHF (without history of COPD) with worse outcomes, however the study was retrospective and was unable to determine causality - in other words, were the patients that received albuterol generally more sick or was their condition worsened by albuterol? No one knows.

That's one of my favorite chicken-and-egg studies--really well done in the most ambiguous fashion, and has absolutely no solid conclusions that anyone can conceivably draw from it. Association studies like this one really shouldn't make it into the literature at all, except to generate further studies, which I guess is the point.

I agree with everyone who's noted that NTG and CPAP are really the mainstay of CHF treatment. Bronchodilators are probably best reserved for people with wheezing on exam or shark fins on capnography, with a possible weak indication for people who aren't moving enough air to hear lung sounds.

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Permalink Reply by Tom Sasso on October 6, 2009 at 9:32pm

Keep in mind another Risk vs. Benifit... the root cause of CHF obviously is a weak heart unable to keep up with demand (unable to "pump" out fluid/keep up enough pressure to keep fluid from pulmonary arteries...). Side effect of Albuterol = increased heart rate. So you just increased the demand (heart rate) in a heart that already can't keep up with demand. But it is a bit like Dopamine in Cardiogenic shock... Dopamine increasing demand so increases infact and possible increase failure... but at the same time increases HR / Contraction so possibly decreasing immediate shock. Albuterol / increased HR may help "pump out" fluid but also increases demand and possibly decreased contraction...
Everything is risk vs. benifit. generally have to look at each case individually.
Good luck and be safe.

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Permalink Reply by blair4630 on October 7, 2009 at 1:58am

As far as the "cardiac asthma" title goes, that's from what I understand, more of a layperson's term for wheezing that has been diagnosed as CHF, where they simply don't understand the physiology behind it, but just know it's cardiac in nature. The statement that comes to mind related to this title is "all that wheezes is not asthma"...which pertains directly to "cardiac asthma".

The train of thought I tend to fall in agreement with is that you are not doing much good to a pt. by opening up the bronchioles when the problem is in the alveoli. And as others have mentioned, adding a positive chronotrope to an already failing heart isn't usually a good idea. NTG and CPAP are the mainstays of treatment in PA (we have state protocols, so that blanket statement is accurate).

Side note on protocols...Furosemide is still on the menu, but only matching an I.V. dose of the pt.'s equivelent daily dose. ie: 1mg lasix I.V.P. for 1mg lasix daily, or x20 for demedex, or x40 for bumex....the idea I believe behind this is that if they are not on a diuretic, then chances are the failure is acute onset from MI or another etiology that hasn't been building up over days, weeks, months, etc., and therefore there isn't enough fluid overload in the system to benefit from lasix, it's purely a pump problem....if they are already on a diuretic, then they probably are exacerbated from fluid overload, and the lasix will help.

You will sometimes see the "shotgun" approach where albuterol and NTG/lasix will be given all together so no diagnosis is missed...but I think most consider this a bad move. (esp. if you're totally off and it's pneumonia). That's the one nice thing about CPAP...even if you're not sure and don't know what drugs to give, CPAP is appropriate in any of the above mentioned settings.

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Permalink Reply by blair4630 on October 7, 2009 at 2:01am

I think the difference between the dopamine and the albuterol in the acute CHF pt. is that with the dopamine, you're kind of between a rock and a hard place. Yes, the heart is taxed, but the shock is going to kill them if you don't do something, and something in this case cannot include supine position or fluids...On the other hand, there are better, much better treatment alternatives to the albuterol.

*Sorry to violate the previously mentioned post etiquette by quoting the whole post, but in this case I was responding to the whole thing.*

Tom Sasso said:

Keep in mind another Risk vs. Benifit... the root cause of CHF obviously is a weak heart unable to keep up with demand (unable to "pump" out fluid/keep up enough pressure to keep fluid from pulmonary arteries...). Side effect of Albuterol = increased heart rate. So you just increased the demand (heart rate) in a heart that already can't keep up with demand. But it is a bit like Dopamine in Cardiogenic shock... Dopamine increasing demand so increases infact and possible increase failure... but at the same time increases HR / Contraction so possibly decreasing immediate shock. Albuterol / increased HR may help "pump out" fluid but also increases demand and possibly decreased contraction...
Everything is risk vs. benifit. generally have to look at each case individually.
Good luck and be safe.

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Permalink Reply by Nathan on October 7, 2009 at 2:25am

"You will sometimes see the "shotgun" approach where albuterol and NTG/lasix will be given all together so no diagnosis is missed...but I think most consider this a bad move. (esp. if you're totally off and it's pneumonia). That's the one nice thing about CPAP...even if you're not sure and don't know what drugs to give, CPAP is appropriate in any of the above mentioned settings."

Just curious, whats really so bad about giving someone lasix when it turns out they have bi lat Pneumonia?

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Permalink Reply by Neil White on October 7, 2009 at 9:07am

As i type this, I openly admit that pharmacology was never my strongest subject at university, but in our patient assessment module and in our OSCES's the differential between CHF and pneumonia was one that was always reinforced... (mainly because the tutor got some pleasure out of trying to trip up students...pressing the arrest button on the sim-man immediately after the student plunges in the furosemide)

I understand that the furosemide will remove excess fluid...leading to quite possibly dehydration. This in turn allows the secretions to further plug the smaller airways...

More importantly for us in the UK it would be a case of giving a drug off licence and outside of prescription rights. You would lose your registration quicker that you could google a defence.

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Permalink Reply by Christopher Ellis on October 7, 2009 at 11:23am

Lasix in a Pneumonia patient can eventually lead to a bad outcome and just for the reasons cited --> small airway mucous plugging and removing liquid secretions that help promote mobilization of mucous. This in the ICU can lead to hypoxia and eventually death. The pulmonologist regularly bronchoscope intubated/trached patient to clean out (small airway mucous plugs) and to help with ventilation and oxygenation.

But with that said mix PMHx patients can have both small airway reactive disease (asthma/copd) and CHF on top of the already boncho-restricted airway.

I always use my physical assessment, PMHx, tools, and vital signs to make a determination on Tx course:

Do they have a PMHx of COPD or CHF
medications?
Was the onset quick or was it over several days?
Fever?
Cough?
Sputum?
Breath Sounds? (can be hard to determine and differentiate between rales/rhonchi/wheezing)
Vital Signs - HTN?

A great tool everyone should have/now be in the back of the rig is capnography. This is going to be a gold standard soon. If someone has bronchospasms they will have a "shark fin" wave form indicting such. True CHF will be hypoxic showing hypercapnia (50 mmHg +).

But remember even with a great assessment and technology making a true diagnosis (especially without chest x-rays and blood work) can be very hard. Thus CPAP (NIPSV) is now the choice for de-compensating CHFers and COPDers. (The Lancet, Volume 356, Issue 9248, Pages 2126 - 2132, 23 December 2000).

So INSTEAD of the shotgun approach (Bronchodilators/Lasix), non-invasive pressure support ventilation (NIPSV) is appropriate when a true Dx cannot be determined.

Neil White said:

As i type this, I openly admit that pharmacology was never my strongest subject at university, but in our patient assessment module and in our OSCES's the differential between CHF and pneumonia was one that was always reinforced... (mainly because the tutor got some pleasure out of trying to trip up students...pressing the arrest button on the sim-man immediately after the student plunges in the furosemide)
I understand that the furosemide will remove excess fluid...leading to quite possibly dehydration. This in turn allows the secretions to further plug the smaller airways...
More importantly for us in the UK it would be a case of giving a drug off licence and outside of prescription rights. You would lose your registration quicker that you could google a defence.

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Permalink Reply by Scott RB on October 7, 2009 at 12:02pm

CHF is not purely the result of a weak heart; the pathophysiology of heart failure is very complex with more than just the heart contributing to the condition (e.g. endocrine and renal systems). And for acute exacerbations, there is multitude of potential causes (from fluid overload to missed medications to MI). The inotropic effects of albuterol are small relative to the many inotropes that exist and the extent to which albuterol can increase the HR varies from person to person (the long term management of CHF frequently includes beta-blockers).

If a patient is wheezing and chronically has CHF (as in it has already been diagnosed), then there is pretty good reason to believe the patient may have a true bronchospastic component to their presentation and that the wheezing is not simply due to bronchial narrowing secondary to edema.

I think we can all agree that when wheezing is not present, the utility of albuterol is questionable, and most likely not needed unless the patient has a history of COPD/asthma, and even then it is best determined on a case by case basis.

If one wants to maximize oxygenation, then albuterol very well may be of benefit to the wheezing CHF patient (at least until better evidence is available). Bethat as it may, I don't think it would be a bad idea to initially institute "standard" CHF therapy and move to bronchodilators further down the line in order to assess for resolution of wheezing with standard treatment.

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