Case 70: A Silent and Rapid Expansion

Natalie Sarafian, Elaine Yu

A 62-year-old male with a history notable for HFrEF (on Lasix), HIV, cirrhosis with varices, ulcerative colitis, methamphetamine use, and Hodgkin’s lymphoma (in remission) presents to the emergency department with acute onset shortness of breath and chest pain. His exertional dyspnea and exertional chest pain are also accompanied with lower extremity edema and orthopnea. Cardiac history is significant for CHF diagnosed in 2020, with a hospitalization in September 2025 for ADHF, and multiple recurrent admissions after being unable to take GDMT medications. Currently, he is adherent but misses medications about once weekly.

Vitals: BP 114/85, HR 103, RR 23, SpO2 94%, BMI 28.98

Physical exam: 2+ pitting edema in lower extremities bilaterally with a venous stasis rash

Labs: Troponin 85. BNPP > 13,000. Cr 1.23. Bilirubin of 1.54.

EKG: normal sinus rhythm with LBBB

A bedside ultrasound was performed:

Figure 1: Parasternal long axis view with severely decreased ejection fraction with trace pericardial effusion.

Figure 2: Parsternal short axis view with global hypokinesia and trace pericardial effusion.

ED Course: Cardiology was paged for the LBBB with troponin leak and heart failure exacerbation, with plan to admit to their service. In the interim, students performed another bedside ultrasound a few hours later for education.

Figure 3: Repeat examination showing increasing size of pericardial effusion.

Discussion:

Pericardial effusion management is routinely taught in medical education and encountered clinically. Pericardial effusions are present in about 6.5% of the general adult population and in 13-20% of high-risk emergency department patients [1]. Given its potential of developing into tamponade and its association with multiple diseases, prompt diagnosis is of utmost importance for proper treatment and prognosis of patients. Cardiac tamponade is an emergent consequence of a rapidly growing pericardial effusion, but it is infrequently encountered, with an incidence of 2 per 1000 people [2]. It is important to note that not all large pericardial effusions will devolve into tamponade; rather, a rapid rate of fluid accumulation creates tamponade [3].

The likelihood of discovering a pericardial effusion changes with a patient’s risk factors and underlying pathology. This patient had multiple comorbidities that are associated with cardiac pathology, including but not limited to CHF, methamphetamine use, HIV, lymphoma, and ulcerative colitis. In a meta-analysis of patients with pulmonary arterial hypertension, myocardial infarction, malignancy, and chronic heart failure, the pooled pericardial effusion prevalence was 19.5% [1]. Although pleural effusions are more common than pericardial effusions in CHF [5], pericardial effusions still demonstrate increased risk for all-cause mortality in CHF patients [6]. Now with antiretroviral therapies, studies have demonstrated low rates of pericardial effusions in HIV-positive outpatients [4]. Finally, the pericardium is a common site for lymphomas to metastasize [7], thus malignant pericardial effusions should also be considered in cancer patients.

Although echocardiograms are the basis of diagnosing pericardial effusions, a patient’s history, examination, EKG, or chest x-ray may raise suspicion [3]. Additionally, bedside ultrasound can also serve as an efficient and noninvasive diagnostic tool. POCUS has been found to reduce time to pericardiocentesis and expedite echocardiograms if indicated [8]. In fact, POCUS can be performed to confirm a pericardial effusion with 96-100% sensitivity and specificity [9]. Furthermore, when pericardial effusions are diagnosed in the emergency department, patients experience shorter hospital stays and reduced mortality [10].

When using POCUS to evaluate for pericardial effusions, measuring the effusion can help approximate the volume. It is important to note that up to 50 mL of fluid is normal and physiologic [10]. If there is clinical concern for tamponade, POCUS should evaluate for right ventricular diastolic collapse, late right atrial diastolic collapse, heart swinging, plethoric IVC, and mitral and tricuspid valve respirophasic flow variation [10]. Once a pericardial effusion and/or cardiac tamponade has been identified and diagnosed, treatment, ranging from conservative management to pericardiocentesis, should be considered.

In this patient’s case, the pericardial effusion was deemed small-moderate by the cardiology service and will be followed up with a formal echocardiogram.

References:

Argulian, E. & Vogel, B. (2024) Evaluation of pericardial effusion. BMJ Publishing Group.
Brown, B., Nigussie, B., Offor, R., & Graham-Hill, S. (2024). Fatal cardiac tamponade: The lethal progression of acute-on-chronic pericardial effusion. Cureus, PMC11264569.
Shanker, D. A., Gaur, A., & Warriner, D. (2025). Pericardial effusion: Overview of aetiology, pathophysiology, diagnosis, and management. Cureus. https://pubmed.ncbi.nlm.nih.gov/41084698/
Lind, A., Reinsch, N., Neuhaus, K., Esser, S., Brockmeyer, N. H., Potthoff, A., Pankuweit, S., Erbel, R., Maisch, B., & Neumann, T. (2011). Pericardial effusion of HIV-infected patients: Results of a prospective multicenter cohort study in the era of antiretroviral therapy. European Journal of Medical Research, 16(11), 480–483. https://pmc.ncbi.nlm.nih.gov/articles/PMC3351804/
Natanzon, A. & Kronzon, I. (2009). Pericardial and pleural effusions in congestive heart failure—Anatomical, pathophysiologic, and clinical considerations. The American Journal of the Medical Sciences, 338(1). https://pubmed.ncbi.nlm.nih.gov/19574887/
Georg M. Fröhlich, Philipp Keller, Florian Schmid, Mathias Wolfrum, Martin Osranek, Christian Falk, Georg Noll, Frank Enseleit, Markus Reinthaler, Pascal Meier, Thomas F. Lüscher, Frank Ruschitzka, Felix C. Tanner, Haemodynamically irrelevant pericardial effusion is associated with increased mortality in patients with chronic heart failure, European Heart Journal, Volume 34, Issue 19, 14 May 2013, Pages 1414–1423, https://doi.org/10.1093/eurheartj/eht006
Mudra, S. E., Rayes, D., Kumar, A. K., Li, J. Z., Njus, M., McGowan, K., Charalampous, C., Kalam, K. A., Syed, A., Majid, M., Schleicher, M., Agrawal, A., Yesilyaprak, A., & Klein, A. L. (2024). Malignant pericardial effusion: A systematic review. CJC Open, 6(8), 967–972. https://pmc.ncbi.nlm.nih.gov/articles/PMC11357784/
Moura de Azevedo, S., Duarte, R., Krowicki, J., Vázquez, D., Pires Ferreira Arroja, S., & Mariz, J. (2024). Heart in focus: Advancing pericardial effusion diagnosis with point-of-care ultrasound. Cureus, 16(12), e76681. https://pmc.ncbi.nlm.nih.gov/articles/PMC11781757/
Merth, T. & Sachdeva, S. (2022). Pericardial effusion and tamponade: Diagnosis and treatment summary. https://emergencycarebc.ca/clinical_resource/clinical-summary/pericardial-effusion-and-tamponade-diagnosisand-treatment-summary/
Rao, V. (2025). POCUS evaluation of pericardial effusion and tamponade. https://www.pocus.org/pocusevaluation-of-pericardial-effusion-and-tamponade/

April 28, 2026April 28, 2026

Case 69: Expedited Workup for a Low-Risk Pulmonary Embolism

Julia Kelly, Cameron Smyres

A 62-year-old man who was recently diagnosed with colon cancer presents to the ED after being diagnosed with a pulmonary embolism on outside CT imaging. The patient had a CT scan of his chest for cancer staging and an incidental PE was found. He was told to seek care at the ED. The patient is asymptomatic, and specifically denies chest pain, dyspnea, acute leg swelling and otherwise feels at his baseline. He denies any recent travel and has no history of blood clots in the past.

Physical Exam: The patient is not in acute distress, lying in bed and breathing comfortably on room air. Lungs are clear to auscultation bilaterally. 1+ pitting edema noted in shins bilaterally. The remainder of the exam is normal.

Labs: CBC with stable chronic macrocytic anemia (Hgb 11.7). CBC, PT and PTT wnl.

**Figure 1:** Parasternal long (no RV dilation)

Video 1: Parasternal short (no D sign present, symmetric squeeze of LV)

ED Course: Limited bedside cardiac ultrasound showed grossly normal heart function, without pericardial effusion or right ventricular dysfunction. No evidence of right heart strain. PE team was consulted who did not recommend formal echocardiogram based on patient’s lack of symptoms, hemodynamic stability, and reassuring bedside ultrasound. Patient was started on Eliquis and referred to PE clinic for outpatient follow up.

Discussion:

Pulmonary embolism (PE) is a potentially life-threatening diagnosis that can present with a variety of symptoms, from asymptomatic to sudden hemodynamic collapse. Approximately half of PEs are diagnosed in the emergency care setting,⁴ making rapid identification and risk stratification especially important. Mortality can reach up to 25-50% in massive PE without prompt treatment. POCUS has been shown to be highly sensitive for large PEs and in those with abnormal vital signs.¹

A rapid bedside tool, POCUS can play an important role in risk stratification of patients with PEs by evaluating for right heart strain, though data shows its utility in diagnosing PE itself might be more limited⁵. Pulmonary emboli block blood flow to the lungs, increasing afterload, leading to right ventricular dysfunction (RVD). RVD is an important prognostic factor and can change management. In this case, bedside echo demonstrated no evidence of right ventricular dysfunction, supporting outpatient management with apixaban and close follow-up; in contrast, evidence of right heart strain may have prompted consideration of more aggressive therapies or inpatient monitoring.

There are several sonographic findings that suggest right heart strain, including RV enlargement (RV:LV ratio), abnormal septal motion such as septal flattening (“D-sign”), and McConnell’s sign (hypokinesis of RV with apical sparing, resembling a flailing sail³). These features reflect acute pressure overload on the RV from a significant pulmonary arterial obstruction. McConnell’s sign is an indication of acute RV strain, rather than chronic changes. Acute RV strain can also be distinguished from chronic overload with the absence of RV hypertrophy.⁵ It is important to note that the sensitivity of POCUS for detecting right heart strain in PE is limited. For example, McConnell’s sign shows high specificity but low sensitivity for acute PE: one study finding a pool estimate of 22% sensitivity and 97% specificity.⁴ Additionally, absence of right heart strain on POCUS does not exclude PE, and CT PE remains the gold standard for definitive diagnosis.

In summary, while POCUS did not reveal right heart strain in this patient with confirmed PE, its use provided timely bedside evaluation of cardiac function that contributed to risk stratification and informed clinical management. This case highlights POCUS’s role as a valuable tool in the assessment of suspected PE.

References

Alerhand S, Sundaram T, Gottlieb M. What are the echocardiographic findings of acute right ventricular strain that suggest pulmonary embolism? Anaesth Crit Care Pain Med. 2021 Apr;40(2):100852. doi: 10.1016/j.accpm.2021.100852. Epub 2021 Mar 26. PMID: 33781986.
Daley JI, Dwyer KH, Grunwald Z, Shaw DL, Stone MB, Schick A, Vrablik M, Kennedy Hall M, Hall J, Liteplo AS, Haney RM, Hun N, Liu R, Moore CL. Increased Sensitivity of Focused Cardiac Ultrasound for Pulmonary Embolism in Emergency Department Patients With Abnormal Vital Signs. Acad Emerg Med. 2019 Nov;26(11):1211-1220. doi: 10.1111/acem.13774. Epub 2019 Sep 27. PMID: 31562679.
Day J BA RDCS. Right Heart Evaluation | Point-of-Care Ultrasound Certification Academy [Internet]. Point-of-Care Ultrasound Certification Academy. 2023. Available from: https://www.pocus.org/right-heart-evaluation/
Fields JM, Davis J, Girson L, Au A, Potts J, Morgan CJ, Vetter I, Riesenberg LA. Transthoracic Echocardiography for Diagnosing Pulmonary Embolism: A Systematic Review and Meta-Analysis. J Am Soc Echocardiogr. 2017 Jul;30(7):714-723.e4. doi: 10.1016/j.echo.2017.03.004. Epub 2017 May 9. PMID: 28495379.
Rudski LG, Wyman WL, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K, Solomon SD, Schiller NB. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography. J Am Soc Echocardio. 2010;23(7):685-713.

April 26, 2026April 25, 2026

Case 67: D-sign in a Post-Cardiac Surgical Patient

Liz Temple, Colleen Campbell

A 51-year-old male patient with past medical history of mitral valve prolapse s/p complex mitral valve repair with left atrial appendage exclusion and repair of atrial septal defect complicated by perioperative pericarditis was directly admitted to the ICU following outpatient echocardiography findings of new right heart strain. Since his open heart surgery, he began to develop progressive dyspnea on exertion and orthopnea accompanied with dizziness and lightheadedness. His exertional capacity has decreased from 3 miles to 100 yards over one week. He otherwise denied fevers,

chills, abdominal pain, or dysuria. He completed an outpatient echo which showed evidence of new severe RV dysfunction which was new compared to his post-operative echo after his complex cardiac surgery which showed preserved RV function. CT PE was completed to rule out PE and did not show evidence of a clinically significant PE as the cause of his new onset RV dysfunction. Bedside cardiac ultrasound was also performed once the patient arrived to the floor.

Physical Exam:

Gen: well appearing, NAD

HEENT: normocephalic, atraumatic, moist mucous membranes, sclera anicteric, EOMI

CV: WWP, RRR, radial pulses 2+, JVP ~9cm

Resp: no increased work of breathing, no accessory muscle use, speaks in full

sentences, breathing comfortably on RA, CTAB

Abd: soft, nontender, nondistended

Ext: no lower extremity edema

Neuro: moves all limbs spontaneously, no facial asymmetry, no dysarthria, EOMI

Labs: Troponin within normal limits

**Figure 1.** Cardiac POCUS with parasternal long axis showing dilated right ventricle (RV). No evidence of a significant pericardial effusion although there appears to be an echogenic focus on anterior RV free wall.

Figure 2: Parasternal short axis view from formal echocardiogram displaying the “D-sign” of right ventricular strain.

Figure 3: Apical 4-chamber view from formal echocardiogram demonstrating septal bowing into left ventricle most prominently during diastole.

Discussion

The “D-sign” on cardiac POCUS can help to identify right heart strain of varying etiologies, and is often considered a canonical sign for pulmonary embolism. This finding is most clearly visualized using a parasternal short axis view where the left ventricle appears as a D-shaped structure as a result of right ventricular overload which causes the interventricular septum to bow towards the left heart.^1,2

While the D-sign has a high specificity (83%), it has a low sensitivity (53%) for pulmonary embolism. Moreover, there are a series of other underlying etiologies of right heart strain that may be associated with this ultrasound signature apart from pulmonary embolism.³

More specifically, right ventricular strain can be stratified by whether it is a result of pressure overload versus volume overload. In a patient with right ventricular pressure overload, elevated pressures on the right side are present both during systole and diastole, and therefore the left ventricular “D-shape” is present throughout the cardiac cycle. Pathologies that correlate with right ventricular pressure overload include pulmonary embolism, pulmonary hypertension, chronic right hear failure with hypertrophy, left-sided heart failure, and ARDS. Conversely, in patients with right ventricular volume overload, the sequelae of volume overload are most apparent during diastolic filling, so the D-sign is most obvious at end diastole while the left ventricle appears more normal and circular shaped during end-systole.⁴ Conditions that correlate with right ventricular volume overload may include severe tricuspid regurgitation, decompensated heart failure, and excessive volume resuscitation.¹

A quantitative tool that is used to distinguish these forms of overload is the Eccentricity Index which utilizes the cross-sectional measurement of the left ventricular cavity in the parasternal short axis view. The index is a proportion between the measurement of length parallel to the septum (D2) and perpendicular to the septum (D1): EI = D2/D1. An EI>1 is suggestive of the D sign. In settings of pressure overload, the EI will be greater than 1 in systole and diastole. In settings of volume overload, the EI is less than 1 in systole and greater than 1 in diastole (Figure 4).⁵

Figure 4: Eccentricity index calculation to distinguish between right ventricular pressure and volume overload. Source: Pocus 101

In this particular case, it is clear that the interventricular septal bowing is variable throughout the cardiac cycle (Figure 1-3) and the D-sign is most evident at end diastole which would suggest a ‘volume overload’ subset of RV strain. Moreover, the EI follows a pattern consistent with right ventricular volume overload, although this was not measured during the formal echo. The etiology of this volume overload RV strain may have been partly attributed by volume overload as he had an elevated JVD and a plump IVC on formal echo. However, considering the context of his recent open-heart surgery with pericarditis and evidence of RV free wall mobility limitation (Figure 3), there was higher suspicion for external compression or inflammation as the cause of his rapid onset RV dysfunction. A subsequent CT scan suggested evidence of possible pericardial clot resulting in external RV compression. The patient was subsequently scheduled for left and right heart catheterization for further assessment of cardiac pressures as a result of this new onset RV strain on ultrasound before proceeding with further surgical intervention.

This case demonstrates the utility of bedside POCUS and clarity of the D sign as a marker for right ventricular dysfunction, presents the eccentricity index as a tool for distinguishing between pressure and volume overload, and the importance of maintaining a broad differential, beyond pulmonary embolism, for the D-sign on cardiac ultrasound.

References:

Dinh V. The D Sign - Right Heart Strain from Pressure vs Volume Overload. POCUS 101, https://www.pocus101.com/the-d-sign-right-heart-strain-from-pressure-vs-volume-overload/ (accessed October 17, 2025).
Cativo Calderon EH, Mene-Afejuku TO, Valvani R, et al. D-shaped left ventricle, anatomic, and physiologic implications. Case Rep Cardiol 2017; 2017: 4309165.
Fields JM, Davis J, Girson L, et al. Transthoracic echocardiography for diagnosing pulmonary embolism: A systematic review and meta-analysis. J Am Soc Echocardiogr 2017; 30: 714-723.e4.
Tanaka H, Tei C, Nakao S, et al. Diastolic bulging of the interventricular septum toward the left ventricle. An echocardiographic manifestation of negative interventricular pressure gradient between left and right ventricles during diastole. Circulation 1980; 62: 558–563.
Ryan T, Petrovic O, Dillon JC, et al. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol 1985; 5: 918–927.

March 6, 2026March 6, 2026

Case 62: Undifferentiated Hypotension in the setting of Atrial Fibrillation with Rapid Ventricular Response

Lucia Hong, Elaine Yu

A 70-year-old male with a history of cirrhosis, COPD, HTN, T2DM, and large abdominal wall hernia who presented after being found down in his home by a neighbor. Upon arrival, the patient was hypotensive with systolic blood pressures in the 70s and in atrial fibrillation with RVR with heart rates in the 170s. He received 500mL intravenous fluids prior to arrival and was transported on supplemental oxygen. The patient was altered and unable to provide history.

On physical examination, the patient appeared acutely ill and minimally responsive. Mucous membranes were dry. Cardiovascular examination demonstrated tachycardia with an irregular rhythm. Lung examination revealed bilateral breath sounds without focal wheezes or stridor. The abdomen was distended with generalized tenderness and a large non-reducible abdominal wall hernia. Extremities were warm and perfused without significant peripheral edema. Neurologic examination demonstrated altered mental status with intermittent command following and spontaneous movement of all extremities.

Synchronized cardioversion was performed following sedation with fentanyl and midazolam, which resulted in sinus tachycardia with improvement in heart rate and blood pressure.

Vital Signs: BP: 94/62 | HR: 102 | RR: 25 | Temp: 100 °F| SpO₂: 99% on 5L O2

Following cardioversion, RUSH was performed with findings of a small pericardial effusion, a plethoric inferior vena cava with minimal respiratory variation, and abnormal right ventricular wall motion with apparent right ventricular enlargement (Figure 1).

Additionally, intra-abdominal free fluid concerning for ascites was also seen (Figure 2). These findings prompted further evaluation of cardiogenic, obstructive, and distributive shock.

**Figure 1.** Apical 4-chamber view showing right ventricular enlargement with wall motion abnormality characterized as hypokinesia of the right ventricular free wall and contraction at the apex.¹

**Figure 2.** Abdominal ultrasound showing large ascites in the left lower quadrant.²

Labs: WBC 13.3, Hgb 6.9, lactate 2.1, troponin 192 -> 189, D-dimer 26,069

Imaging

CTA PE: No definite pulmonary embolism. Mild volume overload, probably cardiogenic.

CT Abdomen/Pelvis with contrast: 4.7 cm left anterior bladder wall abscess. Large volume ascites.

Discussion

Undifferentiated hypotension in the emergency department presents a diagnostic challenge, particularly in patients with multiple comorbidities and competing etiologies of shock. Rapid Ultrasound in Shock and Hypotension (RUSH) examination has emerged as a critical bedside tool allowing evaluation of physiologic contributors to shock prior to definitive diagnostic testing. The RUSH protocol integrates focused cardiac, vascular, pulmonary, and abdominal ultrasound assessment to assess hypovolemic, distributive, cardiogenic, or obstructive etiologies.³ Incorporation of early bedside ultrasound has been shown to alter the presumed category of shock in up to 50% of patients presenting with nontraumatic hypotension.⁴ RUSH is associated with faster diagnostic clarification and earlier targeted therapy in critically ill emergency department patients.⁵ The utilization of POCUS has demonstrated high specificity for detecting right ventricular strain patterns associated with obstructive shock states.⁶ Furthermore, POCUS can improve evaluation of volume status and reduce potentially harmful fluid overload in critically ill patients.⁷

In this case, the patient presented with hypotension, altered mental status, and atrial fibrillation with RVR. Multiple or mixed shock etiologies were plausible, including septic shock from intra-abdominal infection, cardiogenic shock related to arrhythmia or myocardial injury, and obstructive shock with pulmonary embolism. Additionally, hypovolemia was also considered given an initial Hgb 6.9. Identification of right ventricular wall abnormalities increased clinical suspicion for obstructive pathology, and a subsequent D-dimer was noted to be significantly elevated. CTA PE was completed that ruled out pulmonary embolism and demonstrated volume overload from a likely cardiogenic cause. Further CT images identified a bladder abscess as a source of sepsis. Additionally, RUSH examination findings contributed to cautious fluid administration and prompted consideration of alternative shock mechanisms.

This case highlights how POCUS guides subsequent decision-making. As emphasized in current American College of Emergency Physicians guidelines, POCUS serves as an extension of the physical examination and plays an increasingly central role in the early evaluation of critically ill patients in the emergency department.⁸

References

1. Kansara T, Quesada F, Park H, Ghosh K, Saeed M. McConnell’s Sign Still Holds Its Value: A Lesson Learned From Two Cases. Cureus. 2019;11(11):e6240. doi:10.7759/cureus.6240

2. Zuidewind P. Cirrhosis and portal hypertension. Case study, Radiopaedia.org. Published June 21, 2020. https://radiopaedia.org/cases/cirrhosis-and-portal-hypertension-1

3. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid ultrasound in shock in the evaluation of the critically ill. Emerg Med Clin North Am. 2010;28(1):29–56.

4. Jones AE, Tayal VS, Sullivan DM, Kline JA. Randomized, controlled trial of immediate versus delayed goal-directed ultrasound to identify the cause of nontraumatic hypotension in emergency department patients. Crit Care Med. 2004;32(8):1703–1708.

5. Atkinson PRT, Milne J, Diegelmann L, et al. Does point-of-care ultrasonography improve clinical outcomes in emergency department patients with undifferentiated hypotension? A systematic review and meta-analysis. Resuscitation. 2018;127:1–9.

6. Nazerian P, Vanni S, Volpicelli G, et al. Accuracy of point-of-care multiorgan ultrasonography for the diagnosis of pulmonary embolism. Chest. 2014;145(5):950–957.

7. Marik PE, Monnet X, Teboul JL. Hemodynamic Parameters to Guide Fluid Therapy. Ann Intensive Care. 2011;1:1.

8. American College of Emergency Physicians. Emergency Ultrasound Guidelines. Ann Emerg Med. 2017;69(5):e27–e54.

November 19, 2025November 19, 2025

Case 57: Positional Vertigo in the ED With Incidental Interatrial Shunt on Bubble Study

Carmon Controy, Akash Desai

44 y.o. male, brought by EMS from an outpatient procedure suite after sudden onset vertigo and gait instability following a right TMJ/ CNIII V3 injection. Patient experienced abrupt dizziness described as imbalance with ataxic gait, nausea, and one episode of emesis. The symptoms worsen with head movement/position change and improve at rest. No focal weakness, speech change, or headache reported.

Pertinent PMHx: HIV on ART; cognitive impairment on donepezil/memantine; lumbar stenosis s/p L5–S1 decompression. Prior episodes concerning for TIAs/CVAs.

Pertinent FHx: Patient states his father had a “hereditary hole in his heart” which was an incidental finding in his adult life, corrected with surgery.

Vitals on Arrival: BP 146/88, HR 91, RR 16, SpO₂ 98% RA, afebrile

Physical Examination:

General: No distress.
Neuro: Alert/oriented; cranial nerves grossly intact; strength/sensation intact; left-beating nystagmus noted initially; abnormal ataxic gait on arrival.
Cardiopulmonary/Abdomen: Unremarkable.

ED Imaging and Tests:

CT/CTA Head & Neck (stroke protocol): No hemorrhage, large territorial infarct, LVO, or significant stenosis.
MRI Brain (DWI): “Questionable subtle punctate” diffusion restriction in the left thalamocapsular region—artifact favored; tiny acute ischemic focus possible. No hemorrhage or mass effect.
Neurology Consult: Vertigo most consistent with peripheral cause (positional trigger, brief episodes, improvement). HINTS/Dix-Hallpike negative when re-examined after symptom improvement.
Labs: CBC/BMP/coags unremarkable.
Cardiac Ultrasound: Transthoracic Echo with Agitated Saline (Bubble Study)
- Normal LV size and EF ~54%; mild concentric LVH; normal RV size/function; no significant valvular disease.
- Bubble study positive: At rest, microbubbles appeared after 6–7 cardiac cycles; with Valsalva, a large, uncountable shower of bubbles traversed to the left heart—consistent with an interatrial shunt (e.g., PFO/ASD).

ED Course

Symptomatic therapy was provided (e.g., meclizine). Neurological symptoms improved during observation. Neurology judged low suspicion for central vertigo; recommended Epley if recurrent and discharge if symptoms resolved. Comprehensive stroke labs and imaging obtained. TTE with bubble study was positive for interatrial shunt as above, prompting recommendation for outpatient follow-up (stroke clinic/cardiology) to risk-stratify and discuss closure versus medical management in the context of prior suspected cerebrovascular events.

Clinical course and neurology consultant assessment favored positional peripheral vertigo (likely posterior canal BPPV precipitated by head positioning during the OP nerve block procedure) over central causes; neuroimaging was equivocal for a tiny thalamocapsular DWI focus. However, the positive bubble study establishes an interatrial right-to-left shunt, providing a plausible pathway for paradoxical embolism. In a patient with a reported history of likely TIAs/CVAs (including possible TIA at the time of current evaluation), this finding heightens stroke risk considerations and may influence long-term secondary prevention (antithrombotic strategy) and candidacy for shunt closure after more thorough outpatient stroke-neurology/cardiology evaluation.

Discussion

This presentation is most consistent with peripheral, positional vertigo; the positive agitated-saline study is therefore best viewed as incidental to today’s symptoms.¹,² That said, a PFO is common (~20–25% of adults) and provides a plausible conduit for paradoxical embolism (especially when shunting becomes prominent with Valsalva), so its relevance is probabilistic and depends on clinical context rather than timing alone.³,² Frameworks like the Risk of Paraxodical Embolism (RoPE) score weigh age, event phenotype, and vascular risk factors to estimate whether a PFO is likely pathogenic versus incidental.⁴,⁵ Larger shunt burden and high-risk anatomy (e.g., atrial septal aneurysm) increase suspicion, while alternative mechanisms (occult AF, atherosclerosis, dissection, thrombophilia) must be assessed in parallel.⁶,⁵

For secondary cerebrovascular prevention, guideline-concordant work-up (e.g., rhythm monitoring for AF; targeted DVT evaluation; selective hypercoagulability testing) should inform therapy.⁷,⁶ In carefully selected patients 18–60 with a recent non-lacunar ischemic stroke of undetermined cause and a high-risk PFO, randomized trials (RESPECT long-term, CLOSE, REDUCE) show reduced recurrent stroke with percutaneous closure plus antiplatelet therapy compared with antiplatelet therapy alone, albeit with a small increase in atrial arrhythmias;⁸,⁹,¹⁰,¹¹ outside these criteria, optimized medical therapy is appropriate and decisions should be shared between stroke neurology and cardiology.⁶ Bottom line: (1) the PFO is likely incidental to this vertigo episode; (2) given prior TIAs/CVAs without a clear alternative mechanism, the PFO may have contributed to earlier events; and (3) the finding warrants formal risk stratification and guideline-based discussion of closure vs. medical therapy.⁴,⁵,⁶

References

Collins S, Guntheroth WG, Raghu G, et al. Agitated saline contrast echocardiography: Contraindications, complications, and safety. J Am Soc Echocardiogr. 2022;35(1):13-21. doi:10.1016/j.echo.2021.10.016

Abdelmoneim SS, Mulvagh SL, Porter TR, et al. The clinical applications of ultrasonic enhancing agents in echocardiography: 2018 American Society of Echocardiography guidelines update. J Am Soc Echocardiogr. 2018;31(3):241-274. doi:10.1016/j.echo.2017.11.013

Hagen PT, Scholz DG, Edwards WD. Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clin Proc. 1984;59(1):17-20. doi:10.1016/S0025-6196(12)60336-X

Kent DM, Ruthazer R, Weimar C, et al. An index to identify stroke-related vs incidental patent foramen ovale in cryptogenic stroke. Ann Intern Med. 2013;158(5):285-292. doi:10.7326/0003-4819-158-5-201303050-00004

Kent DM, Dahabreh IJ, Ruthazer R, et al. Device closure of patent foramen ovale in patients with cryptogenic stroke: RoPE-estimated attributable fraction and treatment effect. Stroke. 2020;51(7):2143-2150. doi:10.1161/STROKEAHA.119.028966

Kleindorfer DO, Towfighi A, Chaturvedi S, et al. 2021 Guideline for the prevention of stroke in patients with stroke and transient ischemic attack. Stroke. 2021;52(7):e364-e467. doi:10.1161/STR.0000000000000375

Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2014;45(7):2160-2236. doi:10.1161/STR.0000000000000024

Saver JL, Mattle HP, Thaler DE. Patent foramen ovale closure versus medical therapy for cryptogenic ischemic stroke: a topical review. Stroke. 2018;49(6):1541-1548. doi:10.1161/STROKEAHA.117.018153

Saver JL, Carroll JD, Thaler DE, et al. Long-term outcomes of patent foramen ovale closure or medical therapy after stroke. N Engl J Med. 2017;377(11):1022-1032. doi:10.1056/NEJMoa1610057

Mas J-L, Derumeaux G, Guillon B, et al. Patent foramen ovale closure or anticoagulation vs. antiplatelet therapy after stroke (CLOSE). N Engl J Med. 2017;377(11):1011-1021. doi:10.1056/NEJMoa1705915

Søndergaard L, Kasner SE, Rhodes JF, et al. Patent foramen ovale closure or antiplatelet therapy for cryptogenic stroke (REDUCE). N Engl J Med. 2017;377(11):1033-1042. doi:10.1056/NEJMoa1707404

July 11, 2025June 10, 2025

Case 51: Utility of the Spine Sign in Detecting Pleural Effusion on POCUS

John Hermez

A 74 year-old male with a past medical history of metastatic castration-resistant prostate cancer complicated by cauda equina necessitating laminectomy decompression, chronic RLE DVT on apixaban and chronic hypotension presented to the emergency department accompanied by his spouse for altered mental status. Per the patient’s wife, he experienced cognitive decline and increasing weakness for one week prior to presentation. Two days prior to his arrival in the ED, the patient became more confused and agitated with his wife reporting that he appeared to be hallucinating intermittently. While he typically ambulates without assistance and straight-catheterizes himself, he has been unable to care for himself independently.

Physical Exam:

On exam, the patient is in no acute distress and is oriented only to his name. He has diffuse anasarca with 2+ right lower extremity edema and 1+ left lower extremity edema. He is not pale or cyanotic and has shallow respirations on room air with diminished lung sounds and a flat JVP.

Labs: WBC 25.7 and initial lactate 2.2. Hb 9.5 PLT 98, Urine cloudy and orange, growth pending

ECG: NSR at 82 bpm with occasional PVCs, no evidence of ST changes

CXR: Compared to prior, there are new heterogenous bibasilar lung opacities and atelectasis possibly representing pneumonia. No definite pleural effusion or pneumothorax. Stable cardiac silhouette.

To clarify cardiac function and better characterize pulmonary status, a bedside point of care echocardiography was performed.

Figure 1: Trace pericardial effusion seen on parasternal short axis view.

Figure 2: Sagittal right sview demonstrating the thoracic spine sign

Discussion:

Radiographic imaging of the thorax is routinely performed in the ED to aid in the diagnosis of a wide range of cardiopulmonary manifestations. While upright chest x-rays are the Gold Standard for detecting pneumonia in patients, the detection of pleural effusion may be less clearly visualized. Meta-analysis has shown that the screening sensitivity of ultrasound may be 94% as compared to 51% for chest x-ray, in spite of having similar specificity.¹ In this case, we rapidly obtained a point-of-care echocardiogram and pulmonary ultrasound to guide medical decision making in a patient with advanced metastatic disease and anasarca with equivocal radiograph.

A parasternal short axis view was obtained (figure 1) and demonstrated a trace pericardial effusion estimated to be 3mm without evidence of gross systolic dysfunction. Although the right ventricle was poorly visualized during diastole, the small volume of effusion and history of chronic hypotension was reassuring against tamponade physiology. Acquisition of a right subcostal view (figure 2) demonstrated the thoracic spine sign which is a reliable indicator of pleural effusion or hemothorax.²

Figure 3: Subcostal view labelled to identify anechoic pleural effusion (image courtesy of Stanford Medicine 25)⁵

The spine sign is a sonographic description of the visualization of vertebral bodies above the level of the diaphragm, which indirectly indicates that a thoracic fluid collection is present. When there is no thoracic free fluid present, an abrupt loss of the vertebral bodies occurs at the diaphragm due to air in the lungs impeding transmission.² Pleural effusions and traumatic hemothorax can both represent fluid collections, hence the utility of subcostal imaging in the eFAST exam to evaluate thoracic trauma. One study on closed chest trauma has shown the absence of the spine sign to have a negative predictive value of 97.8% in assessing pleural effusion.³ The focused use of ultrasonography in the emergency department is regarded of high value in the early detection and diagnosis of multiple pathologies. Algorithmic exams such as the RUSH protocol provide rapid feedback on the physiology of a critically ill patient which can guide management and are recommended both by the American College of Emergency Physicians and Critical Care Societies.⁴ The potential applications of ultrasonography in resource-limited, austere environments by prehospital personnel are also of particular interest given novel advancements in AI-technology and focused training protocols.

In spite of a technically challenging exam, this case was an excellent example of the utility of multimodal imaging to clarify cardiopulmonary status in the ED. The patient was treated with broad antibiotic therapy for suspected urosepsis and admitted to the hospital for multidisciplinary care. He later was scheduled for therapeutic thoracentesis and surgical evaluation for a scapular fluid collection.

References:

Yousefifard M, Baikpour M, Ghelichkhani P, Asady H, Shahsavari Nia K, Moghadas Jafari A, Hosseini M, Safari S. Screening Performance Characteristic of Ultrasonography and Radiography in Detection of Pleural Effusion; a Meta-Analysis. Emerg (Tehran). 2016 Winter;4(1):1-10. PMID: 26862542; PMCID: PMC4744606.
Dickman, E., Terentiev, V., Likourezos, A., Derman, A. and Haines, L., 2015. Extension of the Thoracic Spine Sign: A New Sonographic Marker of Pleural Effusion. Journal of Ultrasound in Medicine, 34(9), pp.1555-1561.
Vargas CA, Quintero J, Figueroa R, Castro A, Watts FA. Extension of the thoracic spine sign as a diagnostic marker for thoracic trauma. Eur J Trauma Emerg Surg. 2021 Jun;47(3):749-755. doi: 10.1007/s00068-020-01459-1. Epub 2020 Aug 17. PMID: 32803497.
Seif D, Perera P, Mailhot T, Riley D, Mandavia D. Bedside ultrasound in resuscitation and the rapid ultrasound in shock protocol. Crit Care Res Pract. 2012;2012:503254. doi: 10.1155/2012/503254. Epub 2012 Oct 24. PMID: 23133747; PMCID: PMC3485910.
“The Spine Sign.” Edited by Stanford Medicine 25 Bedside Medicine Symposium, Stanford Medicine 25, Stanford Medicine 25 Bedside Medicine Symposium, stanfordmedicine25.stanford.edu/blog/archive/2018/thespinesign1.html. Accessed 25 May 2025.

June 27, 2025June 10, 2025

Case 49: ARDS

Kayhon Rabbani

A 22 year old male who has no past medical history presented with a 3 day history of viral URI-like symptoms with sore throat, dry cough, shortness of breath, and dyspnea on exertion. The patient was an active marine recruit with many other members in his company being sick during this time. Shortly prior to arrival, the patient became unable to walk short flights of steps without becoming short of breath. The patient otherwise had no respiratory or cardiac history. He had no family history of sudden cardiac death or early MI. The patient denied fevers, chills, chest pain, pleuritic chest pain, positional chest pain, abdominal pain, flank pain, dysuria, hematuria, diarrhea, or any other associated symptoms.

Vitals: BP 87/56 | Pulse 96 | Temp 98.6 °F (37 °C) | Resp 28 | SpO2 92%

On physical examination, the patient was alert and in acute distress. Patient presented with tachycardia, hypotension, hypoxia, and tachypnea. Mucous membranes were dry. Respiratory exam revealed decreased air movement, breath sounds, and faint crackles in the right lower lung field.

A bedside echocardiogram was performed.

Figure 1: POCUS echocardiogram in 4 chamber apical view demonstrating a small pericardial effusion.

Figure 2: POCUS lung exam revealed bilateral B lines anterosuperior aspects of the lungs.

Figure 3: Lung consolidation and pleural effusion demonstrating positive "spine sign."

The patient was initially stable but desaturated upon position change. The patient was persistently hypoxic with significant work of breathing on BiPAP before escalating to intubation, remaining persistently hypoxic in the mid 80s post intubation on a ventilator.

Discussion

Acute respiratory distress syndrome (ARDS) is a severe form of acute respiratory failure characterized by rapid onset of widespread inflammation in the lungs. It is defined by the Berlin criteria, which include acute onset within one week of a known clinical insult, bilateral opacities on chest imaging not fully explained by cardiac failure or fluid overload, and severe hypoxemia with a PaO2/FiO2 ratio of less than 300 mmHg.^[1-3]

Common differential diagnoses for ARDS include cardiogenic pulmonary edema, pneumonia, and pulmonary embolism. Cardiogenic pulmonary edema can be differentiated by the presence of signs of fluid overload and cardiac dysfunction, often confirmed by echocardiography. Pneumonia may present with localized infiltrates and clinical signs of infection, while pulmonary embolism typically presents with sudden onset dyspnea, pleuritic chest pain, and may be confirmed by imaging studies such as CT pulmonary angiography.^[1][4-5]

On physical examination, patients with ARDS often present with tachypnea, dyspnea, and diffuse crackles on auscultation. Hypoxemia is a hallmark, and patients may exhibit signs of respiratory distress such as use of accessory muscles and cyanosis. Imaging studies, particularly chest radiography, typically reveal bilateral alveolar infiltrates. Computed tomography (CT) scans can provide more detailed images, showing patchy or diffuse ground-glass opacities and consolidations.^[1-2][6]

Point-of-care ultrasound (POCUS) is a valuable tool in the diagnosis and management of ARDS. Lung ultrasound findings in ARDS include the presence of multiple B-lines (indicating interstitial syndrome), spared areas, pleural line thickening, and subpleural consolidations. Cardiac ultrasound can help differentiate ARDS from cardiogenic pulmonary edema by assessing left ventricular function and the presence of pleural effusions.^[7] Combining lung and cardiac ultrasound can enhance diagnostic accuracy and guide management decisions in critically ill patients with acute hypoxemic respiratory failure.^[7]

References

Saguil, A., & Fargo, M. V. (2020). Acute Respiratory Distress Syndrome: Diagnosis and Management. American family physician, 101(12), 730–738.
Meyer, N. J., Gattinoni, L., & Calfee, C. S. (2021). Acute respiratory distress syndrome. Lancet (London, England), 398(10300), 622–637. https://doi.org/10.1016/S0140-6736(21)00439-6
Matthay, M. A., Zemans, R. L., Zimmerman, G. A., Arabi, Y. M., Beitler, J. R., Mercat, A., Herridge, M., Randolph, A. G., & Calfee, C. S. (2019). Acute respiratory distress syndrome. Nature reviews. Disease primers, 5(1), 18. https://doi.org/10.1038/s41572-019-0069-0
Papazian, L., Calfee, C. S., Chiumello, D., Luyt, C. E., Meyer, N. J., Sekiguchi, H., Matthay, M. A., & Meduri, G. U. (2016). Diagnostic workup for ARDS patients. Intensive care medicine, 42(5), 674–685. https://doi.org/10.1007/s00134-016-4324-5
Sekiguchi, H., Schenck, L. A., Horie, R., Suzuki, J., Lee, E. H., McMenomy, B. P., Chen, T. E., Lekah, A., Mankad, S. V., & Gajic, O. (2015). Critical care ultrasonography differentiates ARDS, pulmonary edema, and other causes in the early course of acute hypoxemic respiratory failure. Chest, 148(4), 912–918. https://doi.org/10.1378/chest.15-0341
Zompatori, M., Ciccarese, F., & Fasano, L. (2014). Overview of current lung imaging in acute respiratory distress syndrome. European respiratory review : an official journal of the European Respiratory Society, 23(134), 519–530. https://doi.org/10.1183/09059180.00001314
Corradi, F., Brusasco, C., & Pelosi, P. (2014). Chest ultrasound in acute respiratory distress syndrome. Current opinion in critical care, 20(1), 98–103. https://doi.org/10.1097/MCC.0000000000000042

November 7, 2024November 12, 2024

Case 35: Intracardiac Mass

Charlotte Ellberg, MD

History:
61-year-old man with a history of asthma, colon cancer s/p hemicolectomy (on Xeloda), COPD, presenting with chief complaint of abdominal pain, non-exertional chest pain, and dyspnea. He denied fever, chills, cough, nausea, vomiting, diarrhea, or dysuria. He was recently hospitalized at an outside hospital for pancreatitis and ascending cholangitis and was treated with antibiotics and underwent an ERCP. He reported that he had completed the antibiotics and was taking rivaroxaban after being told he had a blood clot in his heart. He opted for a patient-directed discharge from that hospital but is re-presenting today for symptoms stated above. His port had been in place since 06/26/2024.

Vitals:
T 98F, HR 87, BP 105/68, RR 16, SpO2 99%

Physical Exam:
Physical exam was notable for no apparent distress, port over right anterior chest without tenderness to palpation, warmth, or erythema. Cardiovascular exam with normal rate, regular rhythm without murmurs, rubs, or gallops. Lungs were clear without crackles or wheezing. Abdomen was soft and non-tender. There was no LE edema.

Labs:
Labs without leukocytosis or anemia
ALT 49
AST 42
ALP 144
T bili 1.38
Troponin within normal limits

A bedside ultrasound was performed.

What do you see?

Figure 1: Apical four chamber view demonstrating hyperechoic mass in right atrium.

Discussion
Bedside ultrasound demonstrated a hyperechoic mass in the right atrium, consistent with records from the outside hospital. A CTPE was also performed which showed no evidence of pulmonary embolism, but did demonstrates a 3.2 cm filling defect in the right atrium corresponding to the previously identified right atrial thrombus at the outside hospital. He also had an abdominal ultrasound which demonstrated a surgically absent gallbladder, no hydronephrosis or calculi, patent portal vein, and no ascites or space occupying lesions. Cardiology was consulted, and given improvement in his symptoms he was discharged with return precautions and recommendations to continue anticoagulation with close follow up for a repeat TTE in the outpatient setting.

Cardiac masses are not common. While they can sometimes present without symptoms, particularly for patients with pacemakers or central lines, they should remain on the differential for patients presenting with unexplained fever, dyspnea, catheter dysfunction, or a new murmur. It is important to recognize catheter associated thrombi as they are associated with increased morbidity and mortality, and can lead to bacteremia, catheter malfunction, SVC syndrome, pulmonary embolism, paradoxical emboli, and prolonged hospitalization and increased cost of care (1).

Specifically within the right atrium, normal anatomy can mimic tumors. The differential for right atrial masses includes benign or malignant neoplasms, myxoma, fibroelastoma, lipoma, cyst, vegetation, or thrombus (2). As demonstrated in this case, pacemaker leads and indwelling catheters in the right atrium can place patients at risk for thrombi or vegetations.1 While this patient had a history of malignancy, it was not known to be metastatic, and the proximity of the mass to the catheter was more suggestive of catheter associated thrombus. Evaluation of right atrial masses includes chest radiography, TTE, and TEE. POCUS is a non-invasive and useful tool that can aid in identifying and visualizing the size, location, and mobility of masses. POCUS can also be utilized to evaluate presence of obstruction or filling defects. Additional evaluation may involve cardiac MRI, computed tomography (CT), or positron emission tomography (PET) to further characterize masses when the etiology remains unclear (3). Management of atrial masses depends on the etiology. In the case of catheter- associated thrombus, management can include anticoagulation, thrombolysis, thrombectomy and eventual removal of the catheter (4).

One prior case report demonstrated the utility of POCUS for quickly diagnosing a catheter associated thrombus, allowing for timely initiation of anticoagulation to prevent further complications such as pulmonary embolism (5). Similarly, this case demonstrates the utility of POCUS in the Emergency Department to identify a recently diagnosed catheter associated thrombus without any significant increase in size or subsequent complications. This allowed for the patient to be discharged in a timely manner and avoid repeating further imaging studies.

1. Geerts W. Central Venous Catheter-Related Thrombosis. http://ashpublications.org/hematology/article-pdf/2014/1/306/1250721/bep00114000306.pdf
2. Sharma S, Narula N, Argulian E. Solving the Diagnostic Challenge of Right Atrial Mass. JACC Case Rep. 2022;4(4):236-238. doi:10.1016/j.jaccas.2022.01.003
3. Parwani P, Co M, Ramesh T, et al. Differentiation of Cardiac Masses by Cardiac Magnetic Resonance Imaging. Curr Cardiovasc Imaging Rep. 2020;13(1). doi:10.1007/s12410-019-9522-4
4. Tran MH, Wilcox T, Tran PN. Catheter-related right atrial thrombosis. Journal of Vascular Access. 2020;21(3):300-307. doi:10.1177/1129729819873851
5. Nelson EL, Greenwood-Ericksen M, Frasure SE. Point-of-care ultrasound diagnosis of a catheter-associated atrial thrombus. Journal of Emergency Medicine. 2016;50(2):e75-e77. doi:10.1016/j.jemermed.2015.06.063

September 28, 2021September 25, 2021

Can Junior EPs Use E-Point Septal Separation to Accurately Estimate Left Ventricular Function?

Background

Point-of-care echocardiography can provide a rapid and accurate assessment of left ventricular function, which is valuable in differentiating causes of hypotension and dyspnea at bedside. Visual estimation of LV function by experienced practitioners has been shown to correlate well with quantitative estimates. However, the number of examinations required before a practitioner is qualified to visually estimate LV function accurately is unknown. Although there are various comparable parameters for assessing LV function, mitral valve E-point septal separation (EPSS) is an easy-to-obtain measurement inversely correlated with LV function. EPSS is an M-mode measurement of the minimum distance between the anterior mitral valve leaflet and the interventricular septum during diastole. Despite its applicability, the reproducibility and accuracy of EPSS as a bedside tool for evaluating LV function in less experienced emergency physicians has yet to be established.

Can Junior Emergency Physicians Use E-Point Septal Separation to Accurately Estimate Left Ventricular Function in Acutely Dyspneic Patients?

Clinical Question

This study aims to determine if novice emergency physicians (PGY 3 and PGY 4) are able to obtain EPSS measurements and determine if these measurements correlate to echocardiographic visual estimations of LV function by experienced emergency physicians.

Methods & Study Design

Design:
Prospective observational study of correlation between EPSS to visual estimation and LV function in patients who present to ED with chief complaint of acute dyspnea.

Population:
Convenience sampling of 70 subjects enrolled in the ED from July 2008 and July 2009. Criteria for enrollment included age > 18 years, chief complaint of dyspnea, ED length > 2 hours, no history of trauma, and normal mental status. Patients with known history of mitral valve repair or replacement, aortic insufficiency, or mitral stenosis were excluded.

Intervention:
12 senior residents (PGY 3 and PGY 4) in EM residency program with variable levels of ultrasound experiences (70 to 150 total ED ultrasound examinations; average of fewer than 25 cardiac examinations) performed transthoracic echocardiogram of patients with chief complaint of acute dyspnea. Ultrasound examination included subcostal, parasternal long axis (PLAX), parasternal short axis, and apical four chamber views. Six-second video clips in parasternal short and long axes were obtained. M-mode measurements of EPSS were recorded in PLAX orientation after all video clips were obtained and calculated during diastole. All examinations were performed without the presence of experienced emergency physicians (EPs).

Outcomes:
One of two experienced EPs reviewed stored video and visually estimated LVEF. Two board-certified cardiologists subsequently reviewed one-half of the video clips and estimated LVEF, blinded to both junior EPs’ EPSS measurements and visual estimations by experienced EPs.

Results

58 out of 70 enrolled subjects had complete echocardiographic studies recorded.

Concordance rates between EPSS measurements by EPs and cardiologist for LVEF were acceptable with kappa for visual LVEF estimation of 0.75 (95% CI = 0.48 to 1.00).

Spearman correlation analysis revealed significant correlation (p = -0.844, p< 0.001) between novice physicians’ measurements of EPSS and visual estimation of LVEF by experienced EPs.

Strengths and Limitations

This study compared EPSS measurement by junior EPs with visual assessment by experienced EPs showing a strong correlation. Experienced EPs were not blinded to results, which may have induced bias, but the authors find this less likely given what they interpret as good agreement on visual estimations between experienced EPs and blinded cardiologists. It is debatable whether the agreement between EPs and cardiologists with kappa of 0.75 represents good agreement. This study utilized a convenience sampling design due to logistical constraints, which may impact the generalizability of its results. Many subjects were excluded for incomplete ultrasound views, but authors note that junior EPs were actually able to assess EPSS for all subjects, further supporting the use of this measurement even when other views are difficult to obtain.

Authors Conclusions

PGY 3 and PGY 4 EM residents were able to obtain measurements of EPSS that correlated closely with visual assessments of LVEF by experienced emergency physicians with extensive point-of-care ultrasound and echocardiography experience. EPSS can serve as a quantitative alternative to visual estimation of LVEF in dyspneic ED patients.

Our Conclusions

Rapid assessment of LVEF with bedside echocardiography can provide useful clinical information in the acutely dyspneic patient. The level of expertise required to accurately visually assess a LVEF is unknown. This study supports EPSS as a useful quantitative addition to visual estimation of LVEF in patients with acute dyspnea for novice emergency physicians with less echocardiography experience. The level of correlation between EPSS and visual estimation was not perfect, suggesting use of EPSS as an addition to rather than replacement for standard visual estimation.

The Bottom Line

EPSS can serve as a quantitative addition to qualitative visual estimation of LVEF with bedside echocardiography, especially for less experienced EM practitioners.

Authors

This post was written by Eugene Han, MS4 at UCSD School of Medicine, with editing by Ben Liotta, MD and Amir Aminlari, MD.

References

1. Secko MA, Lazar JM, Salciccioli LA, Stone MB. Can junior emergency physicians use E-point septal separation to accurately estimate left ventricular function in acutely dyspneic patients? Acad Emerg Med. 2011 Nov;18(11):1223-6. doi: 10.1111/j.1553-2712.2011.01196.x. Epub 2011 Nov 1. PMID: 22044429.
2. McKaigney CJ, Krantz MJ, La Rocque CL, Hurst ND, Buchanan MS, Kendall JL. E-point septal separation: a bedside tool for emergency physician assessment of left ventricular ejection fraction. Am J Emerg Med. 2014 Jun;32(6):493-7. doi: 10.1016/j.ajem.2014.01.045. Epub 2014 Feb 3. PMID: 24630604.
3. Shahgaldi K, Gudmundsson P, Manouras A, Brodin LA, Winter R. Visually estimated ejection fraction by two dimensional and triplane echocardiography is closely correlated with quantitative ejection fraction by real-time three dimensional echocardiography. Cardiovasc Ultrasound. 2009 Aug 25;7:41. doi: 10.1186/1476-7120-7-41. PMID: 19706183; PMCID: PMC2747837.
4. McGowan JH, Cleland JG. Reliability of reporting left ventricular systolic function by echocardiography: a systematic review of 3 methods. Am Heart J. 2003 Sep;146(3):388-97. doi: 10.1016/S0002-8703(03)00248-5. PMID: 12947354.
5. Jacob M, Shokoohi H, Moideen F, Pousson A, Boniface K. An Echocardiography Training Program for Improving the Left Ventricular Function Interpretation in Emergency Department; a Brief Report. Emerg (Tehran). 2017;5(1):e70. Epub 2017 Jun 15. PMID: 29201952; PMCID: PMC5703747.

October 21, 2020May 4, 2021

Identifying regional wall motion abnormalities on ultrasound

Background

Traditionally, the focus of emergency point-of-care echocardiography has been threefold: to assess left ventricular systolic function, to identify the presence of right ventricular enlargement and to evaluate for pericardial effusion. Assessing for regional wall motion abnormalities has been left to formal echocardiography and Cardiology (1). However, structural abnormalities can appear within seconds from the onset of myocardial ischemia (2), so identifying wall motion abnormalities in patients with chest pain or suspected acute coronary syndrome (ACS) in the Emergency Department may be clinically beneficial for emergency providers, leading to more prompt and appropriate diagnostic or therapeutic measures.

We evaluate the following article that looks at whether ED physicians can accurately identify regional wall motion abnormalities.

WAMAMI: emergency physicians can accurately identify wall motion abnormalities in acute myocardial infarction

Clinical Question

Can emergency physicians with basic training in emergency echocardiography accurately identify regional wall motion abnormalities (RWMA) in patients admitted with STEMI?

Methods & Study Design

• Design

Observational report – one group of residents trained and tested in an ultrasound procedure.

• Population

75 patients admitted with STEMI. 6 were excluded from the analysis due to withdrawal, leaving AMA or inability to obtain interpretable images.

• Intervention

Nine residents viewed 2 video instructional modules to provide an introduction to identifying RWMA, and completed an online test evaluating echocardiographic clips for RWMA. They then performed a bedside echocardiogram on patients with known STEMI, though they were blinded to any clinical data about the patient, including the EKG. This was performed within 24 hours of the formal comprehensive echocardiogram.

• Outcomes

The primary outcome was agreement between resident performed echo and formal comprehensive echo on the presence and localization of RWMA.

Results

62% of subjects enrolled had a wall motion abnormality identified by the reference standard. Study investigators identified the presence of RWMA with good sensitivity and specificity (Table 2).

Inter-rater agreement between the point-of-care echocardiogram and the formal echocardiogram for the presence of RWMA was K = 0.79 (95% CI: 0.64–0.94).

Strength & Limitations

Strengths:

Promising results suggest that emergency medicine physicians can be taught to accurately identify RWMA in STEMI with little training. Though the patients in this study were already known to have STEMI on EKG, the application of this procedure may be helpful when patients arrive with NSTEMI or elevated cardiac markers to help in the clinical decision making.

Limitations:

Study was conducted using just 9 residents, and 2 of the residents did the vast majority of the scans. It is possible that these residents are already skilled in ultrasound, so to truly gauge whether this method is broadly teachable, many more residents (with varying levels of baseline ultrasound experience) would need to be evaluated.

Authors Conclusion

The ability to diagnose a RWMA offers emergency clinicians another tool to help manage patients with chest pain and suspected ACS. These data support the introduction of focused training in RWMA identification and expansion of the clinical use of emergency and critical care echocardiography.

Our Conclusion

This is an interesting concept that emergency medicine residents can be trained to successfully identify RWMA using echocardiography. If, and how, this should be implemented in clinical practice is still yet to be explored. Perhaps this could be used in cases of NSTEMI or elevated cardiac markers to help inform clinical decision making, but this study does not answer the question of whether this skill will be clinically useful for ED physicians.

The Bottom Line

It is possible to train emergency medicine physicians to identify regional wall motion abnormalities using echocardiography.

Authors

This post was written by Allison Auchter, MS4 at UCSD School of Medicine, Charles Murchison, MD and Amir Aminlari, MD.

References

P.E. Croft, T.D. Strout, R.M. Kring, et al., WAMAMI: emergency physicians can accurately identify wall motion abnormalities in acute myocardial infarction, American Journal of Emergency Medicine.

1. Cheitlin MD, Armstrong WF, Aurigemma GP, et al. ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASE Committee to Update the 1997 Guidelines of the Clinical Application of Echocardiography). Circulation 2003;108(9):1146–62.
2. Wholgelernter D, Cleman M, Highman HA, et al. Regional myocardial dysfunction during coronary angioplasty: evaluation by two-dimensional echocardiography and 12 lead electrocardiography. J Am Coll Cardiol 1986;7(6):1245.