Albuterol/CHF

Replies to This Discussion

Permalink Reply by Robert Sullivan on October 8, 2009 at 12:02pm

The CHF/COPD/pneumonia diagnosis is one of the most difficult to make. These patients require more critical thinking than almost any other, and poor decisions can do real damage. My philosophy is that the further down the protocol you get, the risk goes up and the potential benefit goes down. CPAP and nitro are very good for CHF. If used on a normo/hypertensive pneumonia patient, nitro won't do that much damage. Lasix can be harmful, and there's less potential benefit from giving it in the field vs. a few hours later in the hospital after an X-ray. I generally don't give Lasix unless a patient's BP is over 180 (not based on evidence, just my experience).

I also think that CPAP lowers the risk of albuterol flooding CHF patients. I'm much less hesitant to try albuterol on borderline wheezing patients if it's being delivered through CPAP.

▶ Reply to This

Permalink Reply by dr-exmedic on October 8, 2009 at 7:23pm

One thing that's missing from this thread is the mention that most CHF patients are not hypervolemic. That used to be the justification for use of Lasix: a pt with a bunch of fluid in his lungs obviously needs to have fluid taken off. But since we've gradually discovered that this isn't true--most CHF pts are euvolemic (and occasionally hypovolemic), even if you ignore the risk of misdiagnosis there's no reason to dehydrate everyone indiscriminately.

▶ Reply to This

Permalink Reply by blair4630 on October 9, 2009 at 5:47am

That's what I referenced when talking about our (I say our, you're from Pitts, right?) current state protocols, that we only use it when there's history of CHF and they're already on a diruetic, as opposed to a new, undiagnosed condition.

dr-exmedic said:

One thing that's missing from this thread is the mention that most CHF patients are not hypervolemic. That used to be the justification for use of Lasix: a pt with a bunch of fluid in his lungs obviously needs to have fluid taken off. But since we've gradually discovered that this isn't true--most CHF pts are euvolemic (and occasionally hypovolemic), even if you ignore the risk of misdiagnosis there's no reason to dehydrate everyone indiscriminately.

▶ Reply to This

Permalink Reply by Tom Bouthillet on October 9, 2009 at 7:30am

But why give it when NTG reduces the preload, takes them out of APE, relieves the shortness of breath, and raises the SpO2? What's the rush?

Tom

▶ Reply to This

Permalink Reply by geoff on October 9, 2009 at 11:39am

Here is a link to an article review by the Medical Director of Ventura County and Santa Barbara County (California) from EMSResponder last year. I've heard some ER Docs say it is worth a try and the next one will say don't do it, I guess that is why it is "practicing medicine".

http://www.emsresponder.com/print/EMS-Magazine/Literature-Review--B...$8227

▶ Reply to This

Permalink Reply by ems rn on October 9, 2009 at 10:18pm

Highly recommend the following article for a great discussion on both the pathophysiology and EMS treatment of HF.

Prehospital Therapy for Acute Congestive Heart failure: State of the Art
Vincent Mosesso, James Dunford, Thomas Blackwell, John Griswell
Univ of Pittsburgh (VM); Univ of CA, San Diego (JD); Carolinas Med Ctr, Mecklenburg EMS, Charlotte, NC (TB); Medstar Amb & Emerg Physicians Adv Bd, Fort Worth, TX (JG).

Prehospital Emergency Care, Volume 7, Issue 1 January 2003, pages 13-23.

Abstract
Acute congestive heart failure (CHF) is one of the most common syndromes encountered in emergency care settings. Correct diagnosis and treatment for pulmonary edema, the most common acute manifestation of CHF, are of primary importance as misdiagnosis can result in deleterious consequences to patients. The pathogenesis of acute pulmonary edema (APE) is currently believed to arise primarily from the redistribution of intravascular fluid to the lungs secondary to acutely elevated left ventricular (LV) filling pressures. This understanding has provided a basis for the management of acute APE, which entails reduction of LV preload, reduction of LV afterload, ventilatory support, inotropic support as needed, and identification and treatment of other underlying factors contributing to elevated LV filling pressures. The agent most applicable and effective for field treatment is nitroglycerin. Diuretics and morphine should be used with caution, as they carry higher risks, especially in misdiagnosed patients. The role of angiotensin-converting enzyme (ACE) inhibitors has yet to be demonstrated in a prehospital setting. Noninvasive positive pressure ventilation methods are effective adjuncts to current treatment, but their mode of delivery presents technical challenges. The development of novel rapid diagnostic tools, currently in progress, might prove valuable for emergency medical services (EMS) personnel in the future. But for now, EMS personnel must rely on their fundamental skills of history taking and physical examination for accurate diagnosis of CHF.

▶ Reply to This

Permalink Reply by Stephanie Ayala on October 26, 2009 at 7:07am

My experience with a "true" CHF pt. went as follows:

73 y/o male picked up from a nursing home with staff saying he was short of breath/low 02 sats. Unfortunately we arrive and he's completely supine with rales and wheezing in all of his fields. Mental status is dementia baseline so it's even more difficult to assess how it's affecting his body, but he is borderline unconscious. Peripheral edema present with JVD and pitting edema (about 2) in his lower calfs. This was at the beginning of my internship. I sat him up repositioned his head a little and went straight for CPAP. No line was established prior to my arrival so after a quick trip to the ambulance I established IV access and administered lasix 40mg IV. His pressure was only in the 110 systolic range so I held off on the nitro to avoid any hemodynamic issues. Within minutes(5-7) his lung fields cleared and he began to mentate better (able to look around, respond to sounds) There was still slight wheezing present but because he had Afib hx I held off on giving a duo-neb through the cpap because of concerns with irritating the heart. CPAP worked wonders for this pt. In our region (upstate NY) lasix is standing orders when peripheral edema is present.
I agree that lasix for a possible pneumonia pt. could be lethal, especially in a geriatric or otherwise high risk pt. It leads to mucus plugging in the smaller airways which will ultimately decrease perfusion. Just wanted to share my story with it. It's interesting to hear about how albuterol might help/hinder the situation; however I feel that if it's going to be used, it should be done through CPAP- for chf pt.'s. If I was ever unsure I would consult with a physician for sure.

▶ Reply to This

Permalink Reply by Mike Rubin on October 26, 2009 at 12:19pm

Stephanie Ayala said:

No line was established prior to my arrival so after a quick trip to the ambulance I established IV access and administered lasix 40mg IV. His pressure was only in the 110 systolic range so I held off on the nitro to avoid any hemodynamic issues.

Glad to hear your pt improved with better positioning and CPAP. If you're concerned about giving NTG to a borderline hypotensive pt, you might want to hold off on the Lasix, too. It's a vasodilator, in addition to a diuretic.

▶ Reply to This

Permalink Reply by kevin davidson on November 4, 2009 at 8:13pm

I can offer this: In acute CHF there is increased pulmonary vascular resistance (PVR) secondary to increased hydrostatic pressure (fluid alveolar edema), narrowed bronchioles from bronchospasm which is a normal physiological response (as seen in drowing for example) and right ventricular overload (backward pressure from fluid, increased PVR, and left ventricular failure/dysfunction to maintain forward flow.) In a nutshell, albuterol possess beta 2 properties which include both bronchial and arteriolar vasodilatory properties (systemically mild) that reduce PVR and thus improve airflow to the alveoli. However, Albuterol also demonstrates beta 1 properties (though mild it varies in person to person) and these include increasing HR and contractility. When a patient is in CHF crisis the beta receptors, both 1 and 2 are under influence of the fight or flight, epi and norepi, which both increase HR and contractility and to some degree promote bronco relaxation. The tricky part is, if it were beta 2 only it would reduce bronchospasm and reduce PVR , both very beneficial. The risk of increasing beta 1 is an issue but albuterol is less of a stimulat here by far than epi. While nitrates are the main stay, the use of albuterol could theoretically be helpful. While caring for patients in an ICU, who had a pulmonary artery catheter placed, which can measure PVR, I did see a reduction in PVR when I administered albuterol in patients with pulmonary edema of both cardiac and non-cardiac (ARDS) and noticed a slight improvement in cardiac output as well. To me, the benefit would probably outweigh the risks (beta 1 stimulation) and would limit it to one treatment. I have reviewed data on this as well, and of note, NTG is more effective than lasix in acute CHF but we tend to use both. Morphine is also effective as it blunts some of the catecholamine surge on beta 1 receptors and reduces preload, but is governed by the BP. I approach it this way, if weezing is heard then albuterol is indicated but, logically as I have discussed the albuterol could help with minimal side effects when wheezing is absent. Incidentally, most experts will tell you that crackles (rales) are also the result of bronchiole constriction in the presence of fluid, the fluid creating a different sound. You could patch and discuss it I suppose and depending on the doc it could go either way. I like your thinking here, shows a desire to help more than the conventional treatment protocals and would suggest to you that this would be an interesting study idea to approach your medical director for and possible publication. You would answer your intriguing question and potentially change mainstream care, just a thought!


While

▶ Reply to This

▶ Reply to This

• First
• Previous
• Next
• Last