Rio Bravo qWeek

ARREAZA: Today we will expand on other treatments for insomnia in adults.

MOIRA: Yes, we spent some time explaining the assessment of insomnia and the first-line treatment, Cognitive Behavioral Therapy for Insomnia (CBT-I). We also mentioned sleep hygiene. You can listen to episode 220 if you want to learn more about that. Medication should be considered a secondary option. The American College of Physicians (ACP) recommends that clinicians use a shared decision-making approach, including a discussion of the benefits, harms, and costs of short-term use of medications, to decide whether to add medication in adults with chronic insomnia disorder in whom CBT-I alone was unsuccessful. 

In general, pharmacotherapy is associated with risks of dependence, tolerance, and poorer quality sleep, whereas evidence-based psychotherapies, like CBT-I, result in better long-term outcomes, no drug dependence or polypharmacy risk, and potential cost savings.

ARREAZA: Yes, we will start this episode by talking about medications. If you practice primary care, I’m 100% sure that a patient has asked you for “sleeping pills” in clinic. Moira, I know our listeners want to hear about meds. What can you tell about meds to treat insomnia?

Moira:We can really split pharmacotherapy for sleep into two categories, OTC, and prescription. And many folks reach for OTC sleep aids before talking to a clinician. When we say OTC sleep aids, we’re mostly talking about sedating antihistamines, like diphenhydramine and doxylamine, which are common in products marketed for occasional sleep difficulties. Melatonin is often marketed as a supplement rather than a drug, but it’s also widely used OTC in many places, though regulations and quality vary by country.

ARREAZA: Exactly. Several studies describe widespread use of these agents among adults and especially older adults, who may face sleep problems related to comorbidities and polypharmacy. Many older adults use OTC sleep aids, often without consulting a healthcare professional or reading labels carefully.

Moira: And there’s evidence that a substantial share of OTC sleep products contains diphenhydramine or doxylamine—first-gen antihistamines that carry anticholinergic burden, which is particularly relevant for older adults. Melatonin’s story is similarly mixed for efficacy. It can modestly affect sleep onset and duration in some populations, especially older adults or circadian rhythm–related sleep problems, but the overall clinical impact is small. What about on the prescription side?

DR. ARREAZA: “Z-drugs” are nonbenzodiazepine sedative-hypnotics that enhance the effects of GABA (neurotransmitter). For example, Zolpidem, Zaleplon, eszopiclone. The risks of benzodiazepine use are significant.Benzodiazepine use is associated with increased fall risk across all age groups, and older adults are the highest risk group. That’s something we should mention to patients who are requesting a “sleeping pill”, “you may sleep a little better, but you may fall.” A meta-analysis of randomized trials in adults over 60 found that benzodiazepines (vs placebo) caused: 2.6× more psychomotor problems (like falls and car accidents), 3.8× more daytime sleepiness, 4.8× more cognitive impairment. Also, benzodiazepine use is associated with a 34% increased risk of hip fractures (RR 1.34) in older adults.

MOIRA: Very significant. Benzodiazepine use is only recommended for four weeks or less due to unproven long-term efficacy and the risk of tolerance, dependence, and misuse. Psychological and physical dependence on benzodiazepines can develop within a few weeks of regular or repeated use. Long-term use is associated with multiple consequences, including dependence, and even increased risk of opioid use. 

Dr ARREAZA: And the withdrawal symptoms are very uncomfortable for benzo dependent patients who try to stop benzos on their own.

MOIRA: And with the Z-drugs you were mentioning, the FDA has required that all Z-drugs carry a Boxed Warning highlighting the risk of complex sleep behaviors such as sleepwalking and sleep-driving, which can result in serious injuries including death. Medications such as benzodiazepines and antidepressants should be avoided for the treatment of insomnia in older adults whenever possible.

DR ARREAZA: There are other prescription options too. Let’s talk about low-dose doxepin has shown to have one of the best balances between efficacy and tolerability. When I hear “doxepin” the word “old” comes to my mind. And, yes, it was approved in 1969, it is a tricyclic antidepressant used to treat depression, anxiety, and insomnia. The recommended dose for insomnia is between 3-6 mg. It is not free of side effects, but lower doses seem to be better tolerated. Complex behaviors associated with doxepin: Doxepin may cause out of bed while not being fully awake and do an activity that you do not know you are doing. The next morning, you may not remember that you did anything during the night. You have a higher chance of doing these activities if you drink alcohol or take other medicines that make you sleepy with this medicine. Reported activities include: "sleep-driving", cooking and eating food, talking on the phone, having sex, or sleepwalking.

Moira: Another group of medications is dual orexin receptor antagonists (DORAs) such as lemborexant are considered medications with good balance of efficacy and tolerability.

No single medication is considered the "best" for all patients. Let’s remember that optimal medication depends on patient age, comorbidities, safety considerations, and the type of insomnia (sleep onset vs. maintenance.)

MOIRA: Older adults deserve special attention. Although insomnia is not a normal part of the aging process, we do see its prevalence increases with age. CBT-I is effective in older adults and is associated with minimal side effects. We can’t talk about sleep meds and older adults without mentioning BEERS criteria, which is a guideline which aims to reduce adverse drug events and polypharmacy by highlighting drugs with risks outweighing benefits, urging safer alternative. In sleep medicine and insomnia management for older adults, Beers Criteria explicitly flag sedating antihistamines (e.g., diphenhydramine, doxylamine) as potentially inappropriate for elderly patients due to anticholinergic burden and adverse effects such as delirium, cognitive impairment, sedation, and falls risk.

MOIRA: Yes! So again, I want to highlight that the first line treatment should always be CBT-I, but when this isn't working or isn't an option, then think about adding pharmacotherapy.

We should really be sharing that OTC options should only be for occasional sleep trouble, not chronic insomnia. Also, be mindful of age-related risks. And consider melatonin with caveats, melatonin may be an option with generally small sleep-onset effects but again, short-term use and quality matters.

To close, OTC sleep aids fill a real need for short-term relief, but they’re not a substitute for diagnosis and evidence-based treatment of insomnia, especially in older adults where safety is a particular concern. And our prescription options like benzos, z drugs, antidepressants, aren’t much better.

DR. ARREAZA: Primum non nocere (“first, do no harm”) is a chief consideration in insomnia management. Sleep is foundational to health, and I hope this helps our colleagues feel more confident in addressing it.If you found this helpful, share it with a friend or colleague and rate us wherever you listen to us. This is Dr. Arreaza, signing off.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week! 

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References:

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Episode 220: Approach of Insomnia in Adults    

ARREAZA: Today we are going to talk about how to approach sleep issues in adults — from the initial assessment all the way through treatment. And I think what is going to surprise a lot of our listeners is the changes in management in recent years, especially what is recommended as first-line therapy. So, let's jump right in.

MOIRA: Sleep is one of those topics that touches every specialty, but Primary Care in particular, so I'm excited to dig into this.

ARREAZA: Let's start with the big picture–statistics. How common are sleep problems in adults?

MOIRA: Incredibly common. Chronic insomnia affects roughly 10% of the general population, and that number has only grown in recent years . During the COVID-19 pandemic, for instance, prevalence rates of insomnia symptoms were reported globally at 20 to 45% (wow). And, importantly, those sleep problems did not simply resolve once infection rates dropped, insomnia symptoms and fatigue have continued even as mood improves in people recovering from COVID-19 infection. 

ARREAZA: Incredible that we are in 2026 and still talking about COVID-19. And we clinicians need to understand that insomnia isn't just an annoyance. It has long-term consequences. Also, financially, insomnia causes direct and indirect costs of up to $100 billion each year.

MOIRA: Exactly. Insomnia is both a risk factor for, and a symptom of, several psychiatric disorders, and it is a predictor of death by suicide, making it an important target for intervention. It's highly comorbid with medical and psychiatric disorders and is associated with significantly increased healthcare utilization and costs. People with insomnia also perform more poorly on complex cognitive tasks. So, we're talking about a condition that affects cognition, mental health, physical health, and quality of life.

ARREAZA: And yet, it still gets overlooked in many clinical encounters. Let’s be honest, dealing with insomnia is not easy on patients… and doctors!

MOIRA: That's the paradox. Primary care practitioners are often poorly informed about sleep disorders, which remain underdiagnosed and sub-optimally managed. In one Italian epidemiological survey, insomnia was reported by 64% of over 3,000 patients interviewed under general practitioners, with 20% reporting both nighttime and daytime symptoms. So, the patients are there, we're just not always asking the right questions or knowing what to do when they tell us about their sleep.

ARREAZA: Great. Let's talk about assessment. In my experience, we need a full encounter to address sleeping issues. Patients tend to mention insomnia as you start walking out of the room. Let’s say a patient tells us, "Doctor, I can't sleep," how de we approach this?

MOIRA: The first step is a comprehensive sleep and health history. Clinical assessment should describe the sleep disturbance and elicit etiological and exacerbating factors. You want to understand the nature of the complaint; is it difficulty to fall asleep, difficulty staying asleep, early morning awakening, or some combination? How long has it been going on? What's the impact on daytime functioning?

ARREAZA: That’s why I think it should be addressed in a full encounter, if possible, because understanding the full extent of the problem requires time. We need to think about contributing factors too.

MOIRA: Absolutely. Factors such as medications, medical disorders, and psychiatric disorders can all increase the risk for insomnia. You need to screen for comorbid conditions, depression, anxiety, PTSD, and chronic pain. Insomnia is actually both a risk factor for and a symptom of several psychiatric disorders. You also want to rule out other primary sleep disorders. Comorbid insomnia and sleep apnea, for example, is highly prevalent and debilitating. If someone has both insomnia and obstructive sleep apnea, treating only one without addressing the other may lead to suboptimal outcomes.

ARREAZA: Now that you mention comorbid conditions, let’s mention nocturia. I feel like it’s very common with my older patients.

MOIRA: Great point. Nocturia (waking from sleep at night to void) and chronic insomnia frequently co-exist in older adults, contributing synergistically to sleep disturbance. Treatments typically target either nocturia or insomnia rather than simultaneously addressing the shared mechanisms for these disorders. There's emerging work on integrated cognitive-behavioral treatment programs that address both conditions simultaneously, which is a promising direction. But at minimum, you should be asking about it, because if nocturia is driving the awakenings, you need to address that as part of the treatment plan.

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References:

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Shivam: My name is Shivam Patel and I’m currently a 3rd year medical student from Western university and today we will be discussing Chronic Pain After Cancer with an emphasis on Improving functionality in cancer survivors and how it overlaps with musculoskeletal dysfunction. We will also talk about the management of pain in outpatient settings as well as the role acute rehab units can play in recovery.

Arreaza: Before getting into specific considerations, let’s start with a framework most clinicians are familiar with, standard, guideline-based management of upper extremity pain.

Typical approach of a patient with shoulder or upper extremity pain

Shivam: The standard approach for any patient coming in with a musculoskeletal issue is stepwise and conservative first. Initial management includes activity modification, NSAIDs or acetaminophen for pain control, and early referral to physical therapy depending on severity and duration. If symptoms persist, we escalate. That may include imaging—usually starting with X-ray, then MRI if indicated, and consideration of corticosteroid injections, particularly for conditions like subacromial impingement or adhesive capsulitis which are commonly seen especially following breast cancer treatment.

Arreaza: Most guidelines emphasize avoiding early imaging unless there are red flags like trauma, neurologic deficits, or suspicion for malignancy or infection. The reason behind this recommendation is that if you image the population of people older than 50 years old, about 40% of people show rotator cuff tears or damage. 

Shivam: When I First heard about this statistic as a medical student, I was shocked and it opened my eyes to the potential downsides of overimaging. We also emphasize maintaining mobility. For example, in adhesive capsulitis, early range-of-motion exercises are key, not immobilization.

Arreaza: Exactly. “Motion is lotion” (Dr. Uy’s mantra).

Shivam: And pharmacologically, we’re moving toward a multimodal approach. NSAIDs are first line when tolerated. Topical agents like diclofenac can be useful. Neuropathic agents like gabapentin or duloxetine are only considered if there’s a neuropathic component.

Arreaza: And a key element is that opioids are not first-line for chronic musculoskeletal pain.

Shivam: Yes, that’s a key point. Current guidelines recommend minimizing opioid use, reserving them for severe, refractory cases, and even then, for short durations with clear treatment goals.

Arreaza: Now, let’s transition this framework into cancer survivors. 

Shivam: The challenge is that many of these patients present with similar complaints. In the upper extremities, for example, they present with shoulder pain, weakness, stiffness, but the underlying causes are more complex.

Particularly in cancer survivors, upper extremity pain is often multifactorial. You still have mechanical issues but layered on top are treatment-related effects such as surgical disruption of anatomy, radiation-induced fibrosis, chemotherapy-induced neuropathy, and generalized deconditioning.

Arreaza: Let’s take an example: THIs a 55-year-old female, s/p left mastectomy and chemoradiation, completed her cancer treatment 1 year ago and now she is presenting with shoulder pain. So, how do we approach this patient?

Shivam: This was a specific case I had the pleasure of familiarizing myself with however it is important to acknowledge just how many patients in America share similar experiences due to the incidence of breast cancer. If we approach this as a typical rotator cuff issue, we might miss key contributors that have been seen in cancer survivors like pectoralis tightness from radiation, scapular dyskinesis from surgery, or even early lymphedema.

Arreaza: Right, and that changes management. Because if you don’t address those underlying contributors, standard treatments may only provide partial or temporary relief.

Shivam: Exactly. And this is where we start to see the limitations of a purely symptom-based approach. Let’s zoom out again. There are nearly 19 million cancer survivors in the U.S., and that number is increasing due to rapidly improving cancer treatment options. With that, we’re seeing more long-term sequelae—especially involving the musculoskeletal system.

Arreaza: Some symptoms in cancer survivors are reduced mobility, persistent fatigue, weakness, and impaired return to activities of daily living. And this may lead to chronic pain and reduced quality of life. 

Shivam: As a side note, we can also acknowledge the impact of mental and psychological aspects on patients who have cancer or any other chronic condition. If they are depressed or less motivated to be active, participate in therapy, the deconditioning effect can be exacerbated in these patients. 

Arreaza: Great point, and also, this is a population that is often under-referred to rehabilitation services. We hope we can increase awareness today.

Shivam: Yes, some sources state that only around 30% of those that qualify for acute rehab are referred to it. Which is surprising, because rehabilitation directly addresses many of these issues that cancer patients experience—strength deficits, mobility limitations, and functional decline.

Arreaza: Let’s talk about pathophysiology for a moment. Why do these patients develop chronic pain?

Shivam: A major factor is deconditioning. During cancer treatment, patients often reduce their activity levels significantly. That leads to loss of muscle mass, decreased endurance, and altered biomechanics.

Arreaza: I see, sarcopenia plays a role in the development of pain in these patients. 

Shivam: And once pain develops, it further limits activity, reinforcing that cycle—pain → inactivity → deconditioning → more pain. On top of that, structural changes, often caused by fibrosis from radiation, reduce tissue elasticity, limit range of motion, and contribute to stiffness and pain.

Arreaza: And neuropathic pain from chemotherapy adds another layer—burning, tingling, or hypersensitivity—which requires a different treatment approach. So, given this complexity, how should we as clinicians adjust our assessment of pain in these patients?

Shivam: I think it’s very important to start with a thorough history to ensure we don’t miss any past history of chronic conditions or intensive treatment for prior medical diagnoses. First, we need to broaden the differential. Don’t assume it’s a single pathology. Second, incorporate function into our assessment. Ask the patient: What can you do? What can’t you do?  Additionally, I think it’s very important to ask what your patient’s goals are for themselves and what they would like to accomplish. 

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References:

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Episode 218: Statin Therapy Fundamentals

What are statins?

Zohal: Statins are medications that lower cholesterol by inhibiting the enzyme HMG-CoA reductase, which prevents cholesterol synthesis in the liver. By doing so, statins decrease low-density lipoprotein cholesterol (LDL-C). 

Why should we lower LDL?

Zohal: There are four main lipoproteins that transport fats in blood, including chylomicrons, VLDL, LDL, and HDL. This is where we get our “bad cholesterol” vs. “good cholesterol”. Of these, LDL is most associated with an increased risk in cardiovascular disease, while a higher HDL is associated with lower risk. Thus, reducing LDL subsequently reduces the risk of cardiovascular disease. 

Arreaza: The lowest LDL I’ve seen was 25, and the highest HDL was 60. HDL doesn’t really have a strict upper limit, but most people fall between 40 and 60. Extremely high HDL—above 100—may not always be protective and can sometimes signal underlying issues.

Zohal: My HDL is 70! Statins are used for both primary prevention, meaning preventing cardiovascular disease before it occurs, and secondary prevention, meaning preventing disease progression in patients who already have cardiovascular disease.

History of statins.

Zohal: In the early 1900’s, researchers were studying the association between cholesterol and atherosclerosis, and at that time, they primarily used animal subjects. These studies were initially not taken seriously, because most believed cardiovascular disease in humans were simply due to aging and was not preventable. 

It wasn’t until the middle of the century when researchers began observing that increased levels of LDL and decreased HDL was correlated with an increased rate of heart attacks. This finding prompted interest in determining the pathway of cholesterol synthesis in the human body. 

Statins were first discovered in the 1970s when researchers identified compounds that inhibit a critical step in cholesterol synthesis. The first statin approved for clinical use was Lovastatin in 1987.

Since then, multiple statins have been developed, including Atorvastatin, Rosuvastatin, Simvastatin, and Pravastatin. Further clinical trials in the 1990s and 2000s showed that statins significantly reduce myocardial infarction, stroke, and cardiovascular mortality.

Why do Statins Matter in Primary Prevention

Zohal: Cardiovascular disease is the most common cause of death worldwide. As previously mentioned, elevated LDL cholesterol contributes to the development of atherosclerotic plaques within arteries, which can lead to heart attack and stroke. By lowering LDL cholesterol and stabilizing plaque formation, statins implemented in a timely manner significantly reduce the risk of atherosclerotic cardiovascular disease.

Arreaza: One of the things I love most about primary care is prevention. You’re working upstream, often quietly, humbly, helping people avoid disease before it starts. And the truth is—you rarely see the full impact of your actions. You don’t get a notification that says, “this patient didn’t have a heart attack because of you.” But every time you help someone control their blood pressure, quit smoking, improve their diet, or stay consistent with their medications, you’re shifting their tracks. You’re reducing risk in ways that may never be fully visible. That’s the paradox and the beauty of it: in primary care, your highest victories are often events that never happen. 

Who Should Receive Statins for Primary Prevention?

Zohal: Recommendations slightly differ depending on who you ask. We look to the U.S. Preventive Services Task Force, the American College of Cardiology, and the American Heart Association for their recommendations regarding statins for primary prevention.

USPSTF on statins.

The U.S. Preventive Services Task Force (or USPSTF for short) is an organization that works to improve the health of people nationwide by making evidence-based recommendations on effective ways to prevent disease & prolong life. They recommend statins for the primary prevention of cardiovascular disease in:

Their recommendations are graded A, B, C, D, and I, depending on the strength of evidence and this is a Grade B recommendation.

Arreaza: So, you have to meet all the criteria to receive a statin, according to USPSTF: 40-75, one CV risk factor and a high 10-y ASCVD score, by the way, the ASCVD risk calculator was introduced in 2013 by AHA/ACC. It is available online for free and many EHRs have integrated this tool into their software. For example, if you use EPIC, you can type .ascvd and get a score automatically. What about patients with a cardiovascular risk less than 10%?

Zohal: For patients with a 7.5–10% risk, some may offer statin therapy on a case-by-case basis as this is a Grade C recommendation. But I’ll get more into this later.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week! 

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References:

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Episode 217: Testicular Cancer

Dr. Arreaza: Welcome to Rio Bravo qWeek Podcast. Today we are discussing testicular cancer, a topic that may not appear frequently in primary care but is extremely important to recognize early. We are joined by Brandon Noorvash and Dr. Ebenezer Dadzie. Please introduce yourselves.

Brandon: Thank you, Dr. Arreaza. My name is Brandon Noorvash. I am a third-year medical student at Western University of Health Sciences with a strong interest in urology.

Ebenezer: Thank you for having us. My name is Dr. Ebenezer Dadzie, and I am a PGY-1 resident in the Clinica Sierra Vista Family Medicine Residency Program.

Dr. Arreaza: Testicular cancer represents about 1-2% of cancers in men, but it is the most common cancer in men between the ages of 15 and 40. The good news is that it is also one of the most curable cancers in medicine, especially when detected early. Let’s start with a quick question for our listeners. If a 25-year-old man presents with a painless lump in his testicle, what diagnosis should immediately come to your mind?

Ebenezer: Testicular cancer should always be high on the differential. While benign conditions can cause scrotal swelling, a painless testicular mass should be considered cancer until proven otherwise.

Dr. Arreaza: I agree. Especially if we perform a physical exam and find that the mass is attached to the testicle. Why is this such an important diagnosis for primary care physicians to recognize, what do you think, Brandon?

Brandon: Testicular cancer typically affects young, otherwise healthy men, and early detection dramatically improves outcomes. Patients may delay seeking care because the lump is painless or because they feel embarrassed discussing symptoms. However, when diagnosed early, the 5-year survival rate exceeds 95%, and in localized disease it approaches 99%.

Dr. Arreaza: Exactly, the survival is incredible and it gets even better with early detection. How common is testicular cancer?

Ebenezer: In the United States, approximately 10,000 new cases are diagnosed each year, with around 500 deaths annually. The relatively low mortality reflects how effective current treatments are, especially chemotherapy for germ cell tumors.

Dr. Arreaza: Let’s talk about risk factors. What should clinicians know about risk factors for testicular cancer? Who is at risk?

Brandon: The most important risk factor is cryptorchidism, or undescended testicle. Men with a history of cryptorchidism have about a 4-to-8-fold increased risk of developing testicular cancer.

Ebenezer: Other risk factors include family history, personal history of testicular cancer, infertility, testicular atrophy, and certain genetic conditions such as Klinefelter syndrome. However, many patients who develop testicular cancer have no clear risk factors.

Dr. Arreaza: Brandon, you recently saw a patient with testicular cancer during your rotation. Can you briefly tell us about that case? Protected health information is not being revealed, so patient confidentiality is being respected during this discussion.

Dr. Arreaza: I think we all were pleasantly surprised to know that lung metastasis did not place the patient in a higher risk category. On the other hand, nonpulmonary visceral metastases (such as liver, bone, or brain) define poor-risk disease in nonseminoma and intermediate-risk disease in seminoma. 

Dr. Arreaza: And of course, if the patient presents with sudden severe pain, we should always think about testicular torsion, which is a surgical emergency. What should clinicians focus on during the physical exam?

Ebenezer: Testicular tumors typically feel firm, irregular, non-tender, and located within the testicle itself.

Brandon: A helpful exam pearl is transillumination. Fluid-filled structures like hydroceles will transilluminate, whereas solid tumors do not.

Dr. Arreaza: I have to admit I’ve never done a transillumination in a scrotum before. 

Brandon/Ebenezer: I’ve done it. I had to clean my pen light afterwards.

Arreaza: Once you suspect testicular cancer, what is the next step in evaluation?

Ebenezer: The first diagnostic test is a scrotal ultrasound. Ultrasound is highly sensitive and can determine whether the mass is intratesticular, which is highly suspicious for malignancy.

Dr. Arreaza: US and tumor markers. Let’s talk a bit more about tumor markers. Why are they useful in testicular cancer?

Brandon: Tumor markers help with diagnosis, staging, and monitoring response to treatment.

Ebenezer: Alpha-fetoprotein, or AFP, is typically elevated in non-seminomatous germ cell tumors, particularly yolk sac tumors. An important point is that pure seminomas do not produce AFP.

Brandon: Beta-hCG can be elevated in both seminomas and non-seminomatous tumors, although the levels are often higher in the non-seminomatous types.

Ebenezer: LDH is less specific but can reflect tumor burden and disease activity, so it’s useful for monitoring progression or response to treatment.

Dr. Arreaza: So, tumor markers are not only diagnostic tools, but they also help guide staging and follow-up care. That’s an important board question. Why don’t we perform a biopsy in a testicular mass? 

Ebenezer: Testicular masses suspicious of cancer are not biopsied because biopsy can disrupt lymphatic drainage and potentially spread tumor cells. Instead, the standard treatment is radical inguinal orchiectomy, which both removes the tumor and establishes the diagnosis.

Dr. Arreaza: Brandon, can you briefly explain the two main categories of testicular cancer?

Brandon: Let’s start with the germ cell tumors. They are broadly divided into seminomas and non-seminomatous germ cell tumors (NSGCT). Seminomas tend to grow more slowly and are highly sensitive to radiation therapy.

Ebenezer: Non-seminomatous tumors include embryonal carcinoma, yolk sac tumor, choriocarcinoma, and teratoma. These tumors tend to be more aggressive but are still highly responsive to treatment.

Dr. Arreaza: How are patients staged once the diagnosis is made?

Ebenezer: Staging typically includes a CT scan of the chest, abdomen, and pelvis to evaluate for metastasis, especially to the retroperitoneal lymph nodes, which are the most common site of spread.

Dr. Arreaza: And how is testicular cancer managed?

Brandon: The initial step is almost always radical inguinal orchiectomy. Depending on staging and tumor type, treatment may include active surveillance, chemotherapy, radiation therapy, or retroperitoneal lymph node dissection.

Ebenezer: One reason outcomes are so favorable is that germ cell tumors respond extremely well to cisplatin-based chemotherapy.

Dr. Arreaza: Let’s talk about prognosis.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

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References:

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Episode 216: Fibromyalgia Overview

Reitta Wyllie and Tejasvi Ayaggari (medical students) discuss with Dr. Arreaza the presentation, diagnosis and management of fibromyalgia, a commonly unrecognized disease that may impact patient’s quality of life if left untreated.  

Written by Reitta Nash, MSIV, American University of the Caribbean. Additional commentary provided by Dr. Tejasvi Ayyagari.  Edits and comments by Hector Arreaza, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Introduction

Fibromyalgia is a chronic pain condition that affects millions of people worldwide, yet it remains one of the most misunderstood disorders in medicine. Patients often experience widespread pain, fatigue, sleep disturbances, cognitive difficulties, and a host of other symptoms that significantly impact daily functioning and quality of life. 

TJ: It’s common, but I feel it is mostly misunderstood and sometimes goes undiagnosed.

Reitta: Yes, despite its prevalence, fibromyalgia has historically been met with skepticism, delayed diagnosis, and stigma. Today, we’ll break down what fibromyalgia is, what we know about its underlying mechanisms, how it’s diagnosed, and how it’s managed using evidence-based approaches.

What is fibromyalgia?

Fibromyalgia is a chronic pain disorder characterized by widespread musculoskeletal pain, accompanied by symptoms such as fatigue, non-restorative sleep, cognitive dysfunction often referred to as “fibro/brain fog,” and mood disturbances.

TJ: Unlike inflammatory or autoimmune diseases, fibromyalgia does not cause structural damage to joints or muscles, nor does it produce objective findings on imaging or routine laboratory testing. Instead, it is considered a centralized pain disorder, meaning pain processing within the central nervous system is altered.

Arreaza: Many years ago, I had a patient who had fibromyalgia in Germany. He shared how hard it was for him to get diagnosed and treated because many countries fail to recognize fibromyalgia as a disease. However, Germany is not one of them. The German Association of the Medical Scientific Societies (AWMF) has established specific diagnostic criteria for fibromyalgia syndrome (FMS). Also, the World Health Organization recognizes fibromyalgia as a chronic condition, and it is included in the International Classification of Diseases 10th edition (ICD-10).

Reitta: The American College of Rheumatology (ACR) recognizes fibromyalgia as a distinct clinical diagnosis, affecting approximately 2–4% of the population, with a higher prevalence in women, though it can affect individuals of any sex or age.

Historical Perspective

Fibromyalgia was once referred to by terms such as fibrositis, a name that implied inflammation of connective tissue. However, as research failed to demonstrate inflammatory changes, the terminology evolved.

In 1990, the American College of Rheumatology introduced the first formal diagnostic criteria, which focused heavily on tender point examination. Over time, these criteria were revised as understanding of the condition improved. Modern diagnostic criteria no longer rely on tender points and instead emphasize symptom severity and widespread pain distribution, reflecting a more patient-centered and clinically practical approach.

What causes fibromyalgia?

The exact cause of fibromyalgia is not fully understood, but current evidence supports a multifactorial, neurobiological model.

The American Academy of Family Physicians identifies a spectrum of chronic overlapping pain conditions that frequently coexist with fibromyalgia, including IBS, TMJ pain, vulvodynia, Chronic fatigue syndrome, interstitial cystitis, endometriosis, chronic tension headaches, migraine, and chronic low back pain. These functional somatic conditions may represent a single disorder manifesting as pain in different body regions at different times over the life span.

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References:

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Abishak and Zat (medical students) explain the cardiotoxic effect of methamphetamine and the diagnosis and treatment of heart failure with reduced ejection fraction (HFrEF). Dr. Arreaza adds insight into the reversibility of meth-associated HFrEF.  

Written by Abishak Govindarajan, MSIV and Zat Akbar Shaw. American University of the Caribbean. Edits and comments by Hector Arreaza, MD.

Welcome

Dr. Arreaza: Welcome to Rio Bravo qWeek. My name is Hector Arreaza, family physician, faculty and associate program director of the Clinica Sierra Vista/Rio Bravo Family Medicine Residency Program. Today we will explore heart failure with reduced ejection fraction, a high-yield and clinically relevant topic in medicine. We will discuss the role of methamphetamine use in the development of HFrEF. This is a pressing issue because about 0.8% of the population 12 and older in the US reported using methamphetamine within the past 12 months in 2024 (National Survey on Drug Use and Health, NSDUH), that’s about ≈2.4 million people!We are joined by two aspiring physicians who will help explore this topic. By the way, we will refer to methamphetamine in this episode as “meth”. [Abishak and Akbar introduce themselves]

Abishak: [Introduce yourself]

The role of meth in HFrEF

Diagnosis

Abishak: Yes, diagnosis requires both symptoms consistent with heart failure and objective evidence of reduced ejection fraction. Echocardiography is the primary diagnostic tool. We also measure BNP. In certain cases, cardiac MRI is used to evaluate myocardial fibrosis and exclude infiltrative or inflammatory etiologies. Coronary angiography may be performed if ischemic disease is suspected.
Guideline-Directed Medical Therapy

Akbar: There are four core pillars in GDMT.

Beta Blocker Considerations

Dr. Arreaza: Yes, the key factor is complete abstinence, plus standard heart failure treatment. If the damage is mostly functional and inflammatory, recovery is possible. If there is extensive fibrosis (scar)

Akbar: Absolutely. Not all meth-associated cardiomyopathy behaves the same way. The extent of fibrosis determines recovery potential. Cardiac MRI with late gadolinium enhancement can help us estimate scar burden. Patients with minimal fibrosis often have better improvement with abstinence and medical therapy.

Dr. Arreaza: So, MRI can actually help us determine the prognosis.

Abishak: Yes, very much so. If MRI shows extensive fibrosis, the likelihood of full EF recovery is lower. That information helps us counsel patients more accurately.

Akbar: Another key issue is right ventricular involvement. Methamphetamine can affect both ventricles. When the right ventricle fails, patients may develop severe peripheral edema, ascites, and hepatic congestion. Right ventricular dysfunction also worsens prognosis significantly.

Dr. Arreaza: And pulmonary hypertension can also worsen the whole picture. 

Akbar: That’s correct. Meth is associated with pulmonary arterial hypertension independently of left-sided heart failure. In some patients, you may see a combined picture of both pulmonary vascular disease and right ventricular dysfunction. That can make management more complicated because pulmonary pressures may remain elevated even after EF improves.

Dr. Arreaza: Tells us about the role of BNP in monitoring these patients. 

Abishak: Serial BNP levels can help track response to therapy. Additionally, troponin may be elevated at times in meth users due to myocardial injury. Monitoring renal function is critical because many heart failure medications affect kidney function and potassium levels.

Akbar:Other lifestyle modifications include sodium restriction, regular follow-ups, vaccination, and avoidance of other cardiotoxic substances such as alcohol or cocaine. Sleep disorders, especially OSA, should be evaluated because untreated OSA worsens heart failure outcomes.

Dr. Arreaza: WhatIs there any role for wearable devices or remote monitoring?

Abishak: Yes, increasingly so. Remote weight monitoring, blood pressure tracking, and symptom reporting can reduce hospitalization. In select patients, implantable hemodynamic monitors may help detect rising filling pressures before symptoms occur.

Dr. Arreaza: It was a great discussion. Thank you, Abishak and Akbar for bringing all that valuable information to us. Let’s wrap it up. 

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Dr. Arreaza:
Welcome back to the podcast. I’m Dr. Arreaza, and today we’re talking about a topic that’s very relevant here in the Central Valley but often not well known in the rest of the country, it is called ValleyFever, or coccidioidomycosis. For more info about the Valley Fever diagnosis and initial treatment, please go to our previous podcast on the subject! Episode 143, recorded by wonderful Dr. Lovedip Kooner.  To help us walk through this, I’m joined by Jordan, a medical student. Jordan, welcome back and Dr. Schlaerth, please introduce yourself. 

Jordan:
Thanks, Dr. Arreaza. This is such an important topic, especially in endemic areas like where we live, the Central Valley of California, and Arizona. The public may think of Valley Fever as a mild pneumonia that just goes away eventually. But that’s not always the case. Some patients develop serious, life-altering complications, and a small but important number develop disseminated disease.

Dr. Arreaza:
Exactly. So today, we’re going to break this down systematically: pulmonary complications, dissemination to other organs, CNS disease, musculoskeletal involvement, systemic symptoms, and then we’ll touch on treatment principles and why follow-up matters so much.

Dr. Schlaerth: Valley Fever can be missed in areas where it is not as common as in the Valley. 1989, earthquake in LA.Pneumonias that is not responding to treatment can be pulmonary cocci.

Dr. Arreaza:
Before we dive into specific complications, let’s zoom out. What percentage of patients get a complicated disease?

Jordan:
So, most infections are self-limited, but about 5–10% of patients develop chronic or progressive pulmonary disease, and 1% develop extrapulmonary disseminated disease. That sounds small, but given how common Valley Fever is in endemic areas, that’s still a lot of people.

Dr. Arreaza:
And the complications can be devastating, and they are not always in primary infection.

Dr. Schlaerth: Dissemination can be silent. We don’t know exactly why dissemination happens; some ethnicities are more susceptible or other groups.

Dr. Arreaza:
Let’s start where Valley Fever usually begins: the lungs. What are the major pulmonary complications clinicians should know about?

Jordan:
The most common long-term complications are chronic pulmonary sequelae. These include: cavitary disease, pulmonary nodules, bronchiectasis, pulmonary fibrosis, and pleural complications like effusions, empyema, or pneumothorax.

Dr. Arreaza:
Cavitary disease comes up a lot. What does that look like clinically?

Jordan:
Cavities form in about 5–15% of cases. Many are asymptomatic, but symptomatic cavities can cause fever, fatigue, cough, sputum production, dyspnea, and hemoptysis. The tricky part is that symptoms often wax and wane, and even with treatment, current antifungals don’t eradicate the organism from chronic cavities.

Dr. Arreaza:
That’s very unfortunate, and sometimes those cavities remain and patients might not know that they have them, and those cavitary lesions may rupture.

Jordan:
Yes, rupture can lead to pyopneumothorax, which is a surgical emergency requiring prompt intervention.

Dr. Kooner: Hello everyone, this is Dr. Kooner, and today I want to talk about one of my favorite topics: coccidioidal cavitary disease—because nothing says “fun lung pathology” like a hole in the lung that refuses to leave.

Coccidioidal cavitary disease is a chronic pulmonary manifestation of infection. Many times, it’s found incidentally on imaging. Sometimes patients are being evaluated for respiratory symptoms, sometimes for systemic complaints, and sometimes for something completely unrelated—like when a chest X-ray was ordered for a pre-op clearance and suddenly… surprise cavity.

Pulmonary cavities develop in about 5-10% of patients with Valley Fever. Most of the time, they appear as thin-walled residual lesions. They can be solitary or multiple, and they can range from a few centimeters to much larger. And while textbooks love to show the “classic look,” in real life they can be a little more… creative.

These cavities can persist for years. Some patients feel completely fine and never know they have one. Others develop chronic symptoms or complications like rupture into the pleural space, secondary infection, or bleeding, which is when everyone suddenly becomes very interested in that cavity.

Here’s an important teaching point: about 20% of patients with cavitary disease also have disseminated infection, most commonly involving bone. This challenges the old-school teaching that cavitary lung disease and dissemination rarely happen together. 

One major risk factor for cavitary disease—and for more severe or complicated infection overall—is diabetes mellitus.

So how do patients usually present?

Symptoms often overlap with classic Valley Fever symptoms. The most common presenting symptoms for cavitary disease that usually trigger evaluation are cough, hemoptysis, fever, and shortness of breath.

Diagnosis and monitoring rely heavily on chest imaging. Plain chest X-rays are usually enough for stable disease. CT scans are typically saved for when you’re worried about complications. Serologic testing is also key, especially complement fixation titers. In general, higher titers correlate with more severe disease and higher relapse risk.

Management depends on symptoms and host factors.
If the patient is asymptomatic and immunocompetent, they often don’t need antifungal therapy. These patients can usually be followed with periodic clinical and imaging monitoring watch closely and don’t panic.

Symptomatic patients are typically treated with oral triazoles, most commonly fluconazole or itraconazole. Treatment is long—usually at least 6 to 12 months, and often longer—because symptoms love to come back once therapy stops. These medications are usually suppressive rather than curative, although newer data suggests triazoles may help with cavity closure in some patients.

Relapses happen in about 25 to 33% of immunocompetent patients, and even more often in immunocompromised patients or transplant recipients. Many of these patients end up needing long-term or even indefinite therapy. Not ideal—but still better than uncontrolled disease.

Surgery still has a role, but it’s more selective now. It’s usually reserved for complications like life-threatening hemoptysis or rupture into the pleural space. Early ruptures might be managed with chest tube drainage. More complicated or delayed cases may need decortication or lung resection.

So, the big picture: symptomatic coccidioidal cavitary disease can be a chronic management challenge. It requires individualized treatment decisions, prolonged therapy for many patients, and long-term follow-up with imaging and serologic monitoring to catch relapses early and prevent complications.

And if there’s one takeaway, it’s this: if you find a stable cavity in someone known to have Valley Fever, sometimes the best move is careful monitoring—not chasing it with endless tests that make everyone nervous, including the patient.

Thanks for listening—and remember, sometimes the lung keeps souvenirs from infections… and sometimes those souvenirs stick around for years. Now, let’s continue with the discussion about pulmonary nodules. This is Dr. Kooner, signing off.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Episode 213: HIV PrEP Review

H. Nicole Magaña, medical student, reviews the history of PrEP and outlines the currently FDA-approved medications used for HIV prevention. Dr. Arreaza provides additional perspective on long-acting injectable options, including how quickly they begin to protect patients after initiation.  

Written by Nicole Magana, MSIV, American University of the Caribbean. Comments and edits by Hector Arreaza, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Pre-exposure prophylaxis for HIV.

Previous episodes related to HIV: 

What is Pre-Exposure prophylaxis (PrEP)?

Pre-exposure prophylaxis, or PrEP, is the use of antiretroviral medications taken by individuals who are HIV-negative to prevent HIV acquisition. There are 30,000 new HIV infections annually in the US. 

How effective is it?

When taken as prescribed, PrEP is highly effective at reducing the risk of HIV transmission through sexual exposure and injection drug use. Patients who are adherent to PrEP can lower their risk of contracting HIV by 99%.

The effectiveness of oral PrEP is highly adherence dependent. In trials with 70% adherence, the relative risk of HIV acquisition was 0.27, compared to 0.51 with 40-70% adherence and no significant benefit with adherence ≤40%.

How does PrEP work?

PrEP works by maintaining therapeutic drug levels in the bloodstream and in target tissues. If HIV exposure occurs, viral replication is inhibited, preventing the establishment of infection.

Brief History of PrEP.

The concept of PrEP originated from early animal studies demonstrating that antiretroviral medications could prevent retroviral transmission when administered before exposure.

In 2010, the iPrEx trial showed that daily oral tenofovir disoproxil fumarate (known as Truvada) with emtricitabine significantly reduced HIV acquisition among men who have sex with men and transgender women. This was the first large clinical trial to demonstrate the effectiveness of PrEP.

In 2012, the FDA approved oral Truvada, which is TDF/FTC (tenofovir disoproxil and emtricitabine) for HIV prevention. Since then, additional studies have expanded indications and introduced new formulations, including long-acting injectable options.

Who Should Be Offered PrEP?

PrEP should be considered for any HIV-negative individual at increased risk of HIV acquisition, including Men who have sex with men, transgender individuals, heterosexual men and women with an HIV-positive partner, individuals with recent bacterial sexually transmitted infections, people who inject drugs, individuals engaging in condomless sex with partners of unknown HIV status.

Remember that PrEP should be offered in a nonjudgmental, patient-centered manner, make it a safe space to talk openly about prevention of HIV. 

Available HIV PrEP Options.

Daily Oral PrEP: There are 2 formulations of Tenofovir. There is Tenofovir disoproxil fumarate (TDF)/ Truvada and Tenofovir alafenamide (TAF)/ Descovy. Each is available in a tablet combined with Emtricitabine a nucleoside reverse transcriptase inhibitor.

Truvada: It is approved for all populations at risk through sexual exposure or injection drug use. Something to look out for before starting this medication is for pre-existing CKD. Do not give to patients who have an estimated glomerular filtration rate of less than 60 mL/min. (6)

Descovy: This option is approved for men who have sex with men and transgender women but is not approved for individuals at risk through receptive vaginal sex. It has less impact on renal function and bone mineral density compared to Truvada. It can be used in moderately reduced kidney function (GFR between 30-60 mL/min).

Truvada and Descovy are taken orally once a day. 

After patients start taking these medications, when are they considered to be protected? 

Nicole: With daily oral PrEP, guidelines differ with WHO and International Aids Society-USA stating it takes about 7 days, while CDC states 21 days to allow for adequate concentration in tissues (1). Adherence is critical for efficacy.

Injectable HIV PrEP.

In 2021, the FDA approved the first Injectable PrEP option Long-acting cabotegravir (CAB-LA)- known on the market as Apretude. Cabotegravir is an integrase strand transfer inhibitor administered as an intramuscular injection.Dosing consists of an initial injection, a second injection one month later, and then maintenance injections every two months (1).

Another option is Lenacapavir (Yeztugo). The Yeztugo as a pre-exposure prophylaxis (PrEP) for HIV in Oct 2024. Yeztugo is the first and only FDA-approved HIV prevention treatment that requires just two injections per year, offering a long-acting option for people who weigh at least 35kg. It is given as 2 injections every 6 months. First dose is given with 2 tablets on Day 1 and Day 2, then every 6 months 2 injections on the same day.

Clinical trials, including HPTN 083 and HPTN 084, demonstrated that injectable cabotegravir is superior to daily oral PrEP in preventing HIV infection. This advantage is largely due to improved adherence rather than differences in intrinsic drug potency.

There have been no head-to-head comparisons between Yeztugo and Apretude, but they are both very effective. Apretude starts protecting 7 days after the first dose, and Yeztugo starts protecting 2 hours after Day 2 (if patient takes the oral loading dose) or 3-4 weeks if no oral load is taken.

Injectable PrEP is particularly beneficial for patients who struggle with daily pill adherence, have trouble swallowing pills, prefer a discreet option, have difficulty storing their medication or have renal or bone disease that limits the use of tenofovir-based regimens like Truvada and Descovy (6). In one unpublished report by Medline, patients who received Apretude had an increase in bone mineral density compared to those who received Truvada (1).

Tests prior to starting PrEP.

Before initiating PrEP, patients must be confirmed to be HIV-negative. Baseline evaluation includes HIV testing with a fourth-generation antigen/antibody assay, HIV RNA testing if acute infection is suspected, renal function testing for oral PrEP, Hepatitis B screening, sexually transmitted infection screening, and pregnancy testing when appropriate. PrEP should not be started in individuals with known or suspected acute HIV infection.

Monitoring for patients on HIV PrEP.

Monitoring typically includes HIV testing every 2 to 3 months, STI screening every 3 to 6 months, renal function monitoring for those on oral PrEP (tenofovir- based), ongoing adherence and risk-reduction counseling. And for injectable PrEP, adherence to the injection schedule is essential, as delayed dosing may increase the risk of resistance if HIV infection occurs.

HIV PrEP is not a prevention for other STIs. Screening for STIs and counseling about prevention is essential.

Breakthrough HIV infections on PrEP are rare and most often associated with poor adherence or delayed diagnosis.

Truvada is more studied in all populations and is considered safe during pregnancy and breastfeeding. There is less data regarding the injectable option in patients who are pregnant, may become pregnant, or whose primary risk factor is injection drug use (1). Injectable PrEP provides an important alternative for patients with chronic kidney disease and bone disease (1).

Key Takeaway

Pre-exposure prophylaxis is a safe, effective, and evidence-based strategy for HIV prevention. With both daily oral and long-acting injectable options available, PrEP can be individualized to meet patient needs. Normalizing PrEP discussions in clinical practice is essential to reducing new HIV infections and advancing public health goals. 

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week! 

References:

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Hyo Mun and Jordan Redden (medical students) explain how to manage HFpEF with medications and touch some basics about nonpharmacologic treatments. Dr. Arreaza asks insightful questions to guide the discussion. 

Written by Hyo Mun, MSIV, American University of the Caribbean; and Jordan Redden, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Treatment of HFpEF

Arreaza: Mike, if you had to name the one therapy everyone with HFpEF should be on, what is it?

Mike: That's easy! SGLT-2 inhibitors. This is the one slam-dunk we have in HFpEF. Empagliflozin (Jardiance) or dapagliflozin (Farxiga) should be started in essentially every patient with HFpEF, and it doesn't matter if they have diabetes or not.

Jordan: And that’s worth repeating, because people still think of these as “diabetes drugs.” They’re not anymore. In HFpEF, SGLT-2 inhibitors reduce heart-failure hospitalizations, improve symptoms, improve quality of life, and even reduce cardiovascular death.

Dr. Arreaza: They’re also simple. Empagliflozin 10 mg daily or dapagliflozin 10 mg daily. No titration, no drama. The effectiveness of these meds was established around 2019 with DAPA-HF and later with DELIVER. These were trials thatdemonstrated that dapagliflozin reduces worsening heart failure and cardiovascular events across the full spectrum of heart failure, from reduced to preserved ejection fraction, independent of diabetes status.

Mike: And the number needed to treat is about 28 to prevent one heart-failure hospitalization. That’s excellent for a disease where we historically had almost nothing that worked.

Jordan: They’re also safe in chronic kidney disease down to an eGFR of about 25, which makes them even more useful in this population.

Dr. Arreaza: Alright. We got SGLT-2 inhibitor, what’s next?

Mike: Volume management. Loop diuretics are still the backbone of symptom control in HFpEF. If the patient is volume overloaded, you diurese, and you diurese aggressively.

Jordan: The goal is euvolemia. Dry weight, no edema, no orthopnea, no waking up gasping for air. A lot of these patients end up needing chronic oral loop diuretics to stay there.

Dr. Arreaza: Something to remember: HFpEF patients don’t tolerate congestion well, and being “a little wet” is not benign. Let’s move into RAAS inhibition. Where do ARBs and ACE inhibitors fit in?

Mike: Between ARBs and ACE inhibitors, ARBs are the winners in HFpEF. They actually reduce heart failure hospitalizations—drugs like candesartan, losartan, valsartan. ACE inhibitors? Not so much. They showed minimal benefit in older HFpEF patients, which is why we go with ARBs instead.

Jordan: But a lot of clinicians get nervous about ACE inhibitors and ARBs because of kidney function, so it’s worth talking through how these drugs actually work in the kidney.

Dr. Arreaza: Yes, misunderstanding may lead to unnecessary drug discontinuation.

Jordan: Under normal conditions, the afferent arteriole brings blood into the glomerulus, and the efferent arteriole is constricted by angiotensin II. That constriction keeps pressure high in the glomerulus and maintains filtration.

Mike: Here's what happens with an ACE inhibitor: you block angiotensin II, the efferent arteriole relaxes, glomerular pressure drops, and GFR dips slightly. Creatinine bumps up a little, and that scares people, but that's actually the whole point—that's how you get kidney protection long-term.

Jordan: High intraglomerular pressure causes hyperfiltration injury and scarring over time. Lowering that pressure protects the kidney long-term. The short-term GFR drop is the price you pay for long-term benefits.

Dr. Arreaza: So let’s talk about CKD, because this is where people panic.

Mike: Right. ACE inhibitors and ARBs are not contraindicated in chronic kidney disease. In fact, they’re recommended even in advanced stages. They reduce progression to kidney failure by about a third.

Jordan: The key is how you use them. Start low. Check creatinine and potassium one to two weeks after starting, then periodically. A creatinine rise up to 30% from baseline is acceptable. That’s not kidney injury, that’s physiology.

Dr. Arreaza: And what about potassium creeping up?

Mike: You adjust the dose or add a potassium binder. You don’t just automatically stop the drug.

Dr. Arreaza: Now there is one absolute contraindication everyone needs to know about! (board exam test)

Jordan: Bilateral renal artery stenosis. This is the big one. In these patients, the kidneys are completely dependent on angiotensin II–mediated efferent constriction to maintain GFR. Take that away, and GFR collapses.

Mike: Creatinine can jump dramatically within days. If you see a creatinine rise of 20% or more shortly after starting an ACE inhibitor, you should be thinking about bilateral renal artery stenosis and stopping the drug immediately.

Dr. Arreaza: After revascularization, though, many patients can tolerate ACE inhibitors again, so this isn’t always permanent. What about cardiorenal syndrome? That’s where things get uncomfortable.

Mike: It is uncomfortable, but cardiorenal syndrome isn't a contraindication. These patients have severe heart failure and kidney disease, and their mortality is actually higher than patients with heart failure alone.

Jordan: ACE inhibitors still reduce mortality and slow kidney disease progression in this group. Studies show that stopping ACE inhibitors during acute heart-failure admissions increases in-hospital mortality three- to four-fold.

Dr. Arreaza: So we are cautious, but we don’t avoid it.

Mike: Exactly. Start low, titrate slowly, monitor labs closely, accept up to a 30% creatinine rise. You only stop if kidney function keeps worsening, or potassium gets dangerously high.

Dr. Arreaza: Alright. Let’s move on. What about mineralocorticoid receptor antagonists… MRA?

Jordan: Spironolactone or eplerenone might reduce hospitalizations in HFpEF, but the data is mixed. This is more of a “select patients” situation.

Mike: And you have to watch potassium and kidney function carefully, especially if they’re already on an ACE inhibitor or ARB.

Dr. Arreaza: What about sacubitril-valsartan, also known as Entresto®?

Mike: Entresto may help patients with mildly reduced EF roughly in the 45 to 57% range. It’s not first-line for HFpEF, but in select patients, it's reasonable.

Dr. Arreaza: Now let’s clarify one of the biggest sources of confusion: beta blockers.

Jordan: Beta blockers are not a treatment for HFpEF itself. They’re only indicated if the patient has another reason to be on them, like coronary disease or atrial fibrillation.

Mike: And timing really matters here. You absolutely do not start beta blockers during acute decompensated heart failure. Their negative inotropic effects can make things worse when patients are volume overloaded.

Jordan: But, and this is critical, you also don’t stop them if the patient is already taking one. Abrupt withdrawal causes a sympathetic surge and dramatically increases mortality.

Dr. Arreaza: If a patient is admitted on a beta blocker, what do we do?

Mike: Continue it at the same dose or reduce it slightly if they’re really unstable. Once they’re euvolemic and stable, you can carefully titrate up.

Jordan: And watch for chronotropic incompetence. HFpEF patients often rely on heart-rate response to exercise, and beta blockers can worsen exercise intolerance.

Dr. Arreaza: Beyond medications, HFpEF is really about treating comorbidities. Aerobic activity can be an initial strategy to improve exercise intolerance and has evidence of improving aerobic function and quality of life. Sodium restriction: improves symptoms, does not decrease risk of death or hospitalizations.

Mike: Hypertension control is huge. For diabetes, the SGLT-2 inhibitors will perform double duty. For obesity, weight loss improves symptoms, and GLP-1 agonists like semaglutide are absolute gamechangers.

Jordan: Don’t forget sleep apnea, atrial fibrillation, and lifestyle. Exercise improves the quality of life, even if it doesn’t change hard outcomes. Lifestyle is the main treatment. 

Dr. Arreaza: And when should you refer to cardiology?

Mike: You should refer when the diagnosis isn't clear; symptoms are not responding to treatment, difficult volume management, end-organ dysfunction, or if you are concerned about advanced heart failure.

Dr. Arreaza: So, it has been a great discussion. What is the takeaway?

Mike: HFpEF treatment isn't about one magic drug -- it's about volume control, SGLT2 inhibitors, smart use of RAAS blockade, and aggressive management of comorbidities.

Jordan: And it's understanding the physiology, so you don’t withhold life-saving therapies out of fear.

Dr. Arreaza: Well said. If you found this helpful, share it with a friend or colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.

Jordan/Mike: Thanks! 

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week! 

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19. Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.
20. Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.
21. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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