In July of 2016, my medical school gave me my first, only, and likely, last stethoscope. Since its adoption by clinicians, it has become so iconic to the physician identity. I wanted to hear murmurs and rales—and sometimes prank my classmates and yell into the diaphragm. Since the start of my clinical rotations, it has been my constant companion, tucked away in my bag until I drape it behind my neck at the start of shift. I felt naked without it. Not in my bag? Might as well show up to work without my scrub top. But here I am, almost 3 years into residency: it’s somewhere at the bottom of my bag…I think.

Throughout the years, emergency clinicians have continued to adapt and evolve in parallel to the rapidly expanding medical device industry, such as portable ultrasounds. The term “portable”, when describing ultrasounds, has evolved beyond most of our wildest imaginations. The once bulky, immobile machines that were only seen in the “ultrasound suite or room” are now stowed away in backpacks and physicians’ back pockets. The ubiquitous nature of ultrasound has encouraged even physicians that did not train with it to adapt and learn to utilize it for almost any chief complaint. 

I posit the adoption of point-of-care ultrasound (POCUS) as part of the routine physical exam in the emergency department. Except in the case of an asthmatic assessment for wheezing, confirmation of breath sounds after rapid sequence induction (RSI), or in a patient with penetrating chest trauma, the stethoscope has become obsolete.

Transthoracic echocardiograms are often the most interesting studies due to the dynamic nature of the exam and the potential for performing various advanced studies. Everyone gets excited seeing a pericardial effusion and making a determination if the patient has early signs of tamponade or the visualization of a transvenous pacemaker wire’s capturing. However, I am arguing for the complete replacement of the stethoscope with point-of-care ultrasound. So, unless you believe in the existence of an I/VI systolic murmur in the patient’s upper left sternal border, you’re probably already convinced of its utility for the cardiac exam. So, let’s talk lungs.

A 32-year-old male presented after a mountain bike accident complaining of shoulder and back pain since he had fallen onto the dirt mound after overestimating a jump. He had been diverted from the trauma bay and moved to the back of the department after having been triaged with an Emergency Severity Index (ESI) of 3. I entered the room and introduced myself. He was tachypneic but easily spoke in full sentences. I placed him on the monitor and found this otherwise healthy, active, and fit male was hypoxic to 90% on room air.

Pneumothorax, right? I just needed to prove it. I set his nasal cannula to 5 liters and continued my physical exam. Breath sounds were normal, trachea was midline, no paradoxical chest wall movement or obvious deformities. On repeat vitals the patient was normotensive, but the pulse oximetry was dipping from 96%, then 94%, then holding at 90%. The nurse immediately called the x-ray technician, however, they were busy with various other trauma patients. My attending brought an ultrasound to the bedside, which revealed no lung sliding on his left. Clearly, he needed a tube thoracostomy performed. Using POCUS, we expedited treatment; the kit was brought to bedside, and by the time the technician had arrived, I had already consented the patient, prepped for the procedure, and anesthetized the site. The tube was placed successfully, and vitals immediately improved. Ultimately, the patient was weaned to 2 liters of oxygen via nasal cannula and admitted to the hospital.

Fast forward to the fall. It was the middle of my second year, and COVID-19 was rearing its head again. But physicians were wiser this time: we ought not to rush to intubate, lest the patient never come off the ventilator. It was mid-afternoon, and the ED staff was pushing through their post-prandial drowsiness. A 64-year-old male with a history of hypertension and medication noncompliance was rushed to the resuscitation bay in respiratory distress. He was in extremis, fluctuating between 80–85%. We put on a non-rebreather and cranked up the oxygen. Using an Egyptian translator, he responded in 2- to 3-word sentences: he reported a recent COVID-19 exposure in his family in Egypt just before returning to the United States and reported the only symptom of shortness of breath.

We listened to his lung fields. We all had differing opinions as to what we were hearing. I reported rales, another reported rhonchi, and the first year medical student said, “[The lungs] sound really bad.” I could not appreciate jugular vein distention (JVD) due to body habitus. He had no lower extremity edema. Blood gas demonstrated no acid-base imbalance. COVID screening was pending. The X-ray technician was on the way. The respiratory technician had put him on a bilevel positive airway pressure machine (BiPAP), but he continued to deteriorate, though more slowly. I was pushed to set up for intubation. But I asked to mix a bag of nitroglycerin first while I took the time to perform an ultrasound. While others argued this was COVID pneumonia, I thought it was due to his hypertension or sympathetic crashing acute pulmonary edema (SCAPE). If I intubate, he codes.

The first blood pressure was taken while I looked at his lungs. B-lines everywhere, systolic greater than 230 and diastolic in the low 100s. While giving myself a pat on the back, I asked the nurse to go ahead and hang the nitroglycerin while keeping him on BiPAP. He stabilized, then headed upstairs to the ICU.

Still not convinced? One more case. A woman in her 70s with a history of congestive heart failure and paroxysmal atrial fibrillation presented complaining of shortness of breath. She had been taking her medications, including her diuretic, as prescribed. She was hypoxic in the mid-80s. After improving her saturations with a nasal cannula, I looked at her monitor and confirmed with an electrocardiogram (EKG): she was also in atrial fibrillation with rapid ventricular response (RVR) in the 130s. She insisted it was due to her fast heart rate. She had been adamant the last time this happened, she was simply given a medication to slow her heart, which caused complete resolution of her symptoms.

Next best step? Is it merely rate control then? Is tachycardia the etiology or symptom? I heard rales bilaterally, measured JVD to the angle of her mandible, and noted 3+ pitting edema to her legs. Ultrasound demonstrated a severely depressed ejection fraction with any pericardial effusion. Her inferior vena cava was plethoric. She had diffuse B lines bilaterally with small pleural effusions. The temptation is simply to rate control. Yet, in taking a step back to further assess, I chose, rather, to drop her preload with noninvasive positive pressure ventilation (NIPPV) and IV diuretics.

In multiple cases, the utilization of POCUS has proven an invaluable tool. I believe it is a vital skill. The emergency physician ought to become comfortable with this tool so readily at our disposal. The next time you feel the need to listen for the difference between rhonchi and rales, pick up a probe to settle the argument.

Author, Aaron Alindogan, MD, is a second year resident at the Department of Emergency Medicine at UT Health San Antonio. Editor, Ryan Joseph, DO, DTM&H, is an assistant professor of emergency medicine at UT Health San Antonio.