Albuterol, CHF, and Pulmonary Edema
Introduction
It seems that every EMS instructor in the world all pull from the same set of war stories and personal anecdotes. I vividly recall every respiratory lecture that even touched on CHF always having the ominous warning that albuterol, by prompting bronchodilation, could prompt flash pulmonary edema. My instructors painted vivid pictures - I walked into every respiratory call from that point on thinking that even a touch of albuterol in a CHF patient would cause flash pulmonary edema and send my otherwise stable patient into a death spiral. My instructors grilled me on using capnography to figure out if my patient was experiencing a CHF or COPD exacerbation. My head spun during scenarios where the patient had both etiologies at play.
I also vividly remember one of my more complicated respiratory calls as a new medic. I had a patient from a low-income part of town telling me that they had both COPD and CHF and had been out of both their usual COPD-focused nebulized medications in addition to their diuretics for CHF. They were bad off, and I had to make a call right then and there. I got the patient into the back of the ambulance, started my basic ALS care, and then placed the patient on CPAP. I heard wheezing and had a somewhat high capnography level. With that, I took my albuterol out and began an in-line nebulizer with the CPAP.
However, I became terrified that I had made the wrong decision as time went on and transport began. I looked down at the patient’s feet and noted their significant pedal edema. I interviewed the patient more on their noncompliance with their diuretics. Terrified that I would cause flash pulmonary edema, I discontinued the albuterol nebulizer. I walked into the ER, gave report to my favorite ER doctor that I gave the patient a partial dose of albuterol, and began restocking.
This particular ER doctor was always interested in educating EMS providers. After his initial stabilizing actions, he pulled me aside, reviewed ultrasound of the heart and echocardiograms, and then told me that the albuterol probably didn’t help the CHFer out. He pointed out that their heart rate was now in the 130s and in afib. For most of my transport, they were sinus in the 80s.
Congestive Heart Failure - A Refresher
Congestive heart failure, put simply, is a failure of the heart to pump effectively and deliver an adequate ejection fraction to the heart. Left ventricular ejection fraction (LVEF) is a percentage used to measure how much blood is pumped out with each contraction of the ventricles. A healthy level is typically around 50-70 percent and decreases slightly as a part of normal aging. Heart failure is officially diagnosed with an LVEF under 40 percent (Malik et al., 2023).
As the name suggests, the heart becomes excessively congested if the left ventricle fails to adequately empty blood with each contraction. Blood begins to pool and back up within the heart. With time, this blood will back up into the peripheral tissues and cause edema in addition to backing up into the pulmonary artery. Venous congestion occurs. Pulmonary hypertension follows as the pulmonary artery attempts to move the excess blood. High venous pressures force blood and plasma fluid out of the capillaries and into the lungs, effectively drowning the alveoli and reducing the available surface for gas exchange.
There are two main types of heart failure - right ventricular heart failure and left ventricular heart failure. For most of this discussion, we are referencing left ventricular heart failure. Left ventricular heart failure typically results in returning blood to the lungs and causes pulmonary edema/congestion. Right ventricular failure typically presents more with peripheral edema as the natural flow of right ventricular congestion causes blood to back up through the right atrium and then back out to systemic circulation.
CHF is one of the most common etiologies responsible for prehospital emergencies, and being ready to treat it with a variety of tools is important. As one of our bread-and-butter call types, EMS providers need to be good at managing CHF complications.
The primary risk factor for CHF development is uncontrolled hypertension that causes excessive ventricular stretch, reduces vascular elasticity, and causes vascular damage over time. CHF is also closely linked with renal failure due to chronic renal hypoperfusion. Other risk factors include a high sodium diet, other cardiac issues such as an MI causing cardiac damage, and smoking.
CHF is most commonly diagnosed off an echocardiogram to assess ejection fraction. In addition, pertinent lab values for CHF include CBC, BMP, and BNP. BNP is a specific hormone produced by the body in response to atrial stretching. During fluid overload states, BNP elevates. An elevated BNP can indicate HF.
Albuterol - A Refresher
Albuterol is one of the first-line medications for most respiratory conditions. It works by stimulating the beta-2 adrenergic receptors, prompting bronchodilation. Opening the bronchi and bronchioles helps improve airflow and improve oxygenation. In asthma, this is particularly helpful; after all, the major issue with asthma is widespread bronchoconstriction that reduces ventilatory capacity and causes hypercapnia. COPD similarly causes hypercapnia through a combination of actual cellular damage to lung parenchyma and chronic, unalleviated bronchoconstriction. However, CHF is a different etiology altogether.
Albuterol & Congestive Heart Failure/Pulmonary Edema - A Complex Relationship
Flash pulmonary edema resulting from albuterol seems to be a common worry in EMS. However, other fields do not seem to share the same attitude. We commonly see patients with CHF as their only respiratory condition discharged with routine nebulizer prescriptions of varying frequency. In addition, respiratory therapy in hospitals commonly makes use of at least some albuterol in the course of treating acute CHF exacerbations even if it is not the mainline therapy.
However - just because it’s used often doesn’t mean it’s the best option for it. The traditional thinking behind albuterol use is that it improves flow and bronchodilates to allow for increased gas exchange. There is another school of thought that albuterol only bronchodilates the already fluid-drenched bronchioles and doesn’t correct the underlying fluid distribution problem. And, to be honest, there is some truth to this. If you look at the JACC sample CHF hospitalization pathway, you will find no mention of routine or even emergent use of beta-2 agonists like albuterol (Maddox et al., 2024). They are not one of the pillars of pharmacological management like diuretics. It is not the recommended standard of care.
CHF & Potassium
Potassium is a critical mineral involved in our muscular contraction and heart function. It is the primary anion involved in the sodium-potassium ion pump, and its outflow of the cell membrane is responsible for allowing depolarization to occur (Pirahanchi et al., 2023). This depolarization is what causes a muscular contraction to take place and for an impulse to be fired (Pirahanchi et al., 2023).
Photo displaying the sodium-potassium pump. Image courtesy of ResearchGate.
Potassium balance is carefully regulated by the kidneys. In a healthy individual, excess potassium is excreted in urine without issue to maintain normal levels. However, CHF and renal damage go hand-in-hand. CHF, as it progresses, will eventually develop systemic hypoperfusion of every organ. The body cannot function effectively without plentiful, oxygen and nutrient-rich blood flowing out of the left ventricle. The kidneys are an extremely vascular and blood-demanding set of organs. With time, CHF perfusion damage will cause prerenal blood flow disruption and cause chronic renal ischemia (Preeti et al., 2016).
By baseline, most CHF patients will present with hypokalemia due to diuretic use and the dilutional effects of being chronically fluid-overloaded (Cunningham & Mehra, 2020). Hyperkalemia typically only occurs during severe, untreated heart failure that has progressed to the point of causing renal hypoperfusion. It is important to remember that CHF itself is not the typical cause of hyperkalemia, but rather its effects of general perfusion damage affecting the kidneys.
Albuterol is a potent potassium shifter, for lack of better words. Studies measuring potassium values before and after albuterol therapy have found that potassium values can drop by as much as 0.6mEq/L in 30 minutes with albuterol use (Erin & Lee, 2017). EMS providers often use this to their benefit when tackling symptomatic, severe hyperkalemia in the prehospital world.
Any rapid change in electrolyte balance is dangerous for fragile CHF patients. In an already borderline-hypokalemic CHF patient, causing further hypokalemia can cause dangerous arrhythmias. Hypokalemia is also associated with muscular weakness, including possible respiratory failure (Castro & Sharma, 2024). In a patient who is already struggling to breathe, we want to avoid this.
CHF & Arrythmias
CHF is strongly associated with atrial fibrillation for a variety of reasons. As the atria become congested and fluid-overloaded, the atria stretch and become irritated. Atrial stretching is a strong driver of ectopi. Fluid overload also worsens the ability of the atria to contract and force blood down into the ventricles, worsening heart failure. As the atria begin to fibrillate, they become even more ineffective at pumping blood throughout the heart normally. Heart function becomes disorganized and worsens ischemia.
Atrial fibrillation also significantly raises the risk of stroke (Lubitz et al., 2010). CHF additionally raises the risk of stroke. Both etiologies increase the risk of embolic stroke due to the venous stasis that occurs in the atria. As the ejection fraction drops, more and more fluid remains within the heart. This fluid has time to coagulate and form emboli. These emboli can become dislodged and enter systemic circulation before lodging in the cerebral circulation.
Fun fact: It is protocol in most hospitals to avoid cardioverting atrial fibrillation patients, if possible, if they are not anticoagulated and have been symptomatic for several days. This is due to the concern of dislodging emboli in the right atrium.
Albuterol and beta-2 agonists in general are arrythmogenic and prompt tachycardia (Wu et al., 2015). A 2015 review found that albuterol use had a 4.8x risk of prompting tachycardia versus the control group (Wu et al., 2015). Prompting tachycardia in a CHF patient may very well cause the onset of atrial fibrillation. This atrial fibrillation can drop cardiac output, worsen ejection fraction due to the heart’s pumping becoming further disorganized, and increase the risk of stroke. We want to avoid doing anything to worsen the cardiac output and respiratory efficacy of a patient who is already struggling to breathe.
Conclusion
The decision to use beta-2 agonists is complicated, controversial, and is best driven by your own local protocols instead of anything I discuss here. However, it is important to have an in-depth understanding of the science behind our interventions and how they work within the body when delivering care. The risk of flash pulmonary edema occurring in a CHF patient who receives beta-2 agonists is largely overstated, but concerns remain with its use due to potassium disturbances and arrhythmias.
References
Castro, D., & Sharma, S. (2024, March 1). Hypokalemia. StatPearls - NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK482465/
Cunningham, J. W., & Mehra, M. R. (2020). Hypokalemia in heart failure: A low or a high point? European Journal of Preventive Cardiology, 28(3), 313–315. https://doi.org/10.1177/2047487320914745
Erin, K., & Lee, C.-S. (2017, February 16). Updated Treatment Options in the Management of Hyperkalemia. US Pharmacist. https://www.uspharmacist.com/article/updated-treatment-options-in-the-management-of-hyperkalemia#:~:text=Use%20of%20albuterol%20has%20been,in%20management%20of%20acute%20bronchospasm.
Lubitz, S. A., Benjamin, E. J., & Ellinor, P. T. (2010). Atrial fibrillation in congestive heart failure. Heart Failure Clinics, 6(2), 187–200. https://doi.org/10.1016/j.hfc.2009.11.001
Maddox, T. M., Januzzi, J. L., Allen, L. A., Breathett, K., Brouse, S., Butler, J., Davis, L. L., Fonarow, G. C., Ibrahim, N. E., Lindenfeld, J., Masoudi, F. A., Motiwala, S. R., Oliveros, E., Walsh, M. N., Wasserman, A., Yancy, C. W., & Youmans, Q. R. (2024). 2024 ACC Expert Consensus Decision Pathway for treatment of heart Failure with reduced ejection Fraction. Journal of the American College of Cardiology, 83(15), 1444–1488. https://doi.org/10.1016/j.jacc.2023.12.024
Malik, A., Brito, D., Vaqar, S., & Chhabra, L. (2023, November 5). Congestive heart failure. StatPearls - NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK430873/
Pirahanchi, Y., Jessu, R., & Aeddula, N. R. (2023, March 13). Physiology, Sodium potassium pump. StatPearls - NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK537088/
Preeti, J., Alexandre, M., Iyngkaran, P., Merlin, T. C., & Claudio, R. (2016). Chronic heart failure and comorbid renal dysfunction - a focus on Type 2 cardiorenal syndrome. Current Cardiology Reviews, 12(3), 186–194. https://doi.org/10.2174/1573403x12666160606120958
Wu, R., Lin, S., & Zhao, H. (2015). Albuterol in the treatment of acute respiratory distress syndrome: A meta-analysis of randomized controlled trials. World Journal of Emergency Medicine, 6(3), 165. https://doi.org/10.5847/wjem.j.1920-8642.2015.03.001
