SonoPro Tips and Tricks for Pulmonary Embolism

Written by: Megan Chenworth, MD (NUEM ‘24) Edited by: Abiye Ibiebele, MD (NUEM ‘21) Expert Commentary by: John Bailitz, MD & Shawn Luo, MD (NUEM ‘22)

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SonoPro Tips and Tricks

Welcome to the NUEM Sono Pro Tips and Tricks Series where Sono Experts team up to take you scanning from good to great for a problem or procedure! For those new to the probe, we recommend first reviewing the basics in the incredible FOAMed Introduction to Bedside Ultrasound Book and 5 Minute Sono. Once you’ve got the basics beat, then read on to learn how to start scanning like a Pro!

Did you know that focused transthoracic cardiac ultrasound (FOCUS) can help identify PE in tachycardic or hypotensive patients? (It has been shown to have a sensitivity of 92% for PE in patients with an HR>100 or SBP<90, and approaches 100% sensitivity in patients with an HR>110 [1]). Have a hemodynamically stable patient with PE and wondering how to risk stratify? FOCUS can identify right heart strain better than biomarkers or CT [2].

Who to FOCUS on?

1. Patients presenting with chest pain or dyspnea without a clear explanation, or with a clinical concern for PE. The classic scenario is a patient with pleuritic chest pain with VTE risk factors such as recent travel or surgery, systemic hormones, unilateral leg swelling, personal or family history of blood clots, or known hypercoagulable state (cancer, pregnancy, rheumatologic conditions).

2. Patients presenting with unexplained tachycardia or dyspnea with VTE risk factors

3. Unstable patients with undifferentiated shock

4. When PE is suspected but CT is not feasible: such as when the patient is too hemodynamically unstable to be moved to the scanner, too morbidly obese to fit on the scanner, or in resource-limited settings where scanners aren’t available

   1. One may argue AKI would be another example of when CT is not feasible (though there is some debate over the risk of true contrast nephropathy - that is a discussion for another blog post!)

How to scan like a Pro

1. Key is to have the patient as supine as possible - this may be difficult in truly dyspneic patients

2. If difficulty obtaining views arise, the left lateral decubitus position helps bring the heart closer to the chest wall

FOCUS on these findings

You only need one to indicate the presence of right heart strain (RHS).

1. Right ventricular dilation

2. Septal flattening: Highly specific for PE (93%) in patients with tachycardia (HR>100) or hypotension (SBP<90) [1]

3. Tricuspid valve regurgitation

4. McConnell’s sign

   • Definition: Akinesis of mid free wall and hypercontractility of apical wall (example below)

   • The most specific component of FOCUS: 99% specific for patients with HR>100bpm or SBP<90 [1]

5. Tricuspid annular plane systolic excursion (TAPSE)

• The most sensitive single component of FOCUS: TASPE < 2cm is 88% sensitive for PE in tachycardic and hypotensive patients; 93% sensitive when HR > 110 [1]

Where to FOCUS

Apical 4 Chamber (A4C) view: your best shot at seeing it all

1. Find the A4C view in the 5th intercostal space in the midclavicular line

2. Optimize your image by sliding up or down rib spaces, sliding more lateral towards the anterior axillary line until you see the apex with the classic 4 chambers - if the TV and MV are out of the plane, rotate the probe until you can see both openings in the same image; if the apex is not in the middle of the screen, slide the probe until the apex is in the middle of the screen. If you are having difficulty with this view, position the patient in the left lateral decubitus.

3. Important findings:

   1. RV dilation: the normal RV: LV ratio in diastole is 0.6:1. If the RV > LV, it is abnormal. (see in the image below)

   2. Septal flattening/bowing is best seen in this view

   3. McConnell’s sign: akinesis of the free wall with preserved apical contractility

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McConnell’s Sign showing akinesis of the free wall with preserved apical contractility

4. Tricuspid regurgitation can be seen with color flow doppler when positioned over the tricuspid valve

Tricuspid regurgitation seen with color doppler flow

5. TAPSE

• Only quantitative measurement in FOCUS, making it the least user-dependent measurement of right heart strain [3]

• A quantitative measure of how well the RV is squeezing. RV squeeze normally causes the tricuspid annulus to move towards the apex.

• Fan to bring the RV as close to the center of the screen as possible

• Using M-mode, position the cursor over the lateral tricuspid annulus (as below)

• Activate M-mode, obtaining an image as below

• Measure from peak to trough of the tracing of the lateral tricuspid annulus

  • Normal >2cm

How to measure TAPSE using ultrasound

Parasternal long axis (PSLA) view - a good second option if you can’t get A4C

1. Find the PSLA view in the 4th intercostal space along the sternal border

2. Optimize your image by sliding up, down, or move laterally through a rib space, by rocking your probe towards or away from the sternum, and by rotating your probe to get all aspects of the anatomy in the plane. The aortic valve and mitral valve should be in plane with each other.

3. Important findings:

   1. RV dilation: the RV should be roughly the same size as the aorta and LA in this view with a 1:1:1 ratio. If RV>Ao/LA, this indicates RHS.

   2. Septal flattening/bowing of the septum into the LV (though more likely seen in PSSA or A4C views)

Right heart strain demonstrated by right ventricle dilation

Parasternal Short Axis (PSSA) view: the second half of PSLA

Starting in the PSLA view, rotate your probe clockwise by 90 degrees to get PSSA

1. Optimize your image by fanning through the heart to find the papillary muscles - both papillary muscles should be in-plane - if they are not, rotate your probe to bring them both into view at the same time

2. Important findings:

   1. Septal flattening/bowing: in PSSA, it is called the “D-sign”.

“D-sign” seen on parasternal short axis view. The LV looks like a “D” in this view, particularly in diastole.

Subxiphoid view: can add extra info to the FOCUS   

1. Start just below the xiphoid process, pointing the probe up and towards the patient’s left shoulder

2. Optimize your image by sliding towards the patient’s right, using the liver as an echogenic window; rotate your probe so both MV and TV are in view in the same image

3. Important findings

   1. Can see plethoric IVC if you fan down to IVC from RA (not part of FOCUS; it is sensitive but not specific to PE)

Plethoric IVC that is sensitive to PE

What to do next?

Sample algorithm for using FOCUS to assess patients with possible PE.

*cannot completely rule out PE, but negative FOCUS makes PE less likely

Limitations to keep in mind:

1. FOCUS is great at finding heart strain, but the lack of right heart strain does not rule out a pulmonary embolism

   1. Systematic review and meta-analysis concluded that the overall sensitivity of FOCUS for PE is 53% (95% CI 45-61%) for all-comers [5]

2. Total FOCUS exam requires adequate PSLA, PSSA, and A4C views – be careful when interpreting inadequate scans

3. Can see similar findings in chronic RHS (pHTN, RHF)

   1. Global thickening of RV (>5mm) can help distinguish chronic from acute RHS

   2. McConell’’s sign is also highly specific for acute RHS, whereas chronic RV failure typically appears globally akinetic/hypokinetic

SonoPro Tips - Where to Learn More

1. Right Heart Strain at 5-Minute Sono: http://5minsono.com/rhs/

2. Ultrasound GEL for Sono Evidence: https://www.ultrasoundgel.org/posts/EJHu_SYvE4oBT4igNHGBrg, https://www.ultrasoundgel.org/posts/OOWIk1H2dePzf_behpaf-Q

3. The Pocus Atlas for real examples: https://www.thepocusatlas.com/echocardiography-2

4. The Evidence Atlas for Sono Evidence: https://www.thepocusatlas.com/ea-echo

References

1. 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.

2. Weekes AJ, Thacker G, Troha D, Johnson AK, Chanler-Berat J, Norton HJ, Runyon M. Diagnostic Accuracy of Right Ventricular Dysfunction Markers in Normotensive Emergency Department Patients With Acute Pulmonary Embolism. Ann Emerg Med. 2016 Sep;68(3):277-91. doi: 10.1016/j.annemergmed.2016.01.027. Epub 2016 Mar 11. PMID: 26973178.

3. Kopecna D, Briongos S, Castillo H, Moreno C, Recio M, Navas P, Lobo JL, Alonso-Gomez A, Obieta-Fresnedo I, Fernández-Golfin C, Zamorano JL, Jiménez D; PROTECT investigators. Interobserver reliability of echocardiography for prognostication of normotensive patients with pulmonary embolism. Cardiovasc Ultrasound. 2014 Aug 4;12:29. doi: 10.1186/1476-7120-12-29. PMID: 25092465; PMCID: PMC4126908.

4. Hugues T, Gibelin PP. Assessment of right ventricular function using echocardiographic speckle tracking of the tricuspid annular motion: comparison with cardiac magnetic resonance. Echocardiography. 2012 Mar;29(3):375; author reply 376. doi: 10.1111/j.1540-8175.2011.01625_1.x. PMID: 22432648.

5. 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;30:714–23.e4.

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Expert Commentary

RV function is a frequently overlooked area on POCUS. Excellent post by Megan looking specifically at RV to identify hemodynamically significant PEs. We typically center our image around the LV, so pay particular attention to adjust your views so the RV is optimized. This may mean moving the footprint more laterally and angle more to the patient’s right on the A4C view. RV: LV ratio is often the first thing you will notice. When looking for a D-ring sign, make sure your PSSA is actually in the true short axis, as a diagonal cross-section may give you a false D-ring sign. TAPSE is a great surrogate for RV systolic function as RV contracts longitudinally. Many patients with pulmonary HTN or advanced chronic lung disease can have chronic RV failure, lack of global RV thickening. Lastly remember, that a positive McConnell’s sign is a great way to distinguish acute RHS from chronic RV failure.

John Bailitz, MD

Vice Chair for Academics, Department of Emergency Medicine

Professor of Emergency Medicine, Feinberg School of Medicine

Northwestern Memorial Hospital

Shawn Luo, MD

PGY4 Resident Physician

Northwestern University Emergency Medicine

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How To Cite This Post:

[Peer-Reviewed, Web Publication] Chenworth, M. Ibiebele, A. (2021 Oct 4). SonoPro Tips and Tricks for Pulmonary Embolism. [NUEM Blog. Expert Commentary by Bailitz, J. Shawn, L.]. Retrieved from http://www.nuemblog.com/blog/sonopro-tips-and-tricks-for-pulmonary-embolism

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Other Posts You May Enjoy

Non-Invasive Positive Pressure Ventilation in the ED

Written by: Matt McCauley, MD (NUEM PGY-2) Edited by: Sarah Sanders, MD, (NUEM PGY-4) Expert commentary by: James Walter, MD

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Noninvasive positive pressure ventilation (NIPPV) refers to the delivery of positive pressure ventilator support without the insertion of an endotracheal tube [1]. This intervention works to improve lung volumes and decrease the work of breathing, making it a practical tool in the management of acute respiratory failure [2]. Due to the multitude of indications, it is important for emergency physicians to understand both the ventilator settings of NIPPV devices and the types of respiratory failure they address. 

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Fig 1

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Approach to the Patient

The utilization of NIPPV requires active management by the EM provider. One cannot simply set the patient on initial settings of “ten over five” and walk away; both subjective criteria (eg patient comfort, patient mental status, and degree of air leak around mask) and objective data (eg O2 saturation, respiratory rate, pH, PaCo2) must be taken into account. The provider can start promoting success at the initiation of treatment by starting at low settings and talking the patient through the procedure, both of which can improve compliance [5]. If time permits, baseline blood gases obtained at this point can be useful in monitoring clinical course [10].

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Fig 2

Different etiologies of respiratory failure, as described in Figure 2, require different approaches to the titration of ventilator settings. In the case of a patient with an acute exacerbation of COPD, the clinician should initially adjust FiO2 to an O2 saturation of 88-92%, taking care to avoid chasing high saturations that can paradoxically increase shunt, decrease respiratory drive, and subsequently promote patient deterioration. Arterial blood gas measurements should then be taken at thirty minutes and then trended over 1-2 hours of therapy [5]. If the patient continues to demonstrate failure to blow off CO2 or has not improved tidal volumes, ventilation can be improved by increasing IPAP alone while keeping EPAP constant, thereby improving tidal volumes, oxygenation, and CO2 retention [7,10].

Patients with pulmonary edema exhibit type 1 failure and require a different approach. The pathophysiology of pulmonary edema causes alveoli to be less available for gas exchange as the lungs are filled with fluid, leading to a shunt physiology with alveoli being perfused but not able to oxygenate or ventilate. This shunt physiology manifests itself as a low O2 saturation despite the use of 100% FiO2. This requires an increase in mean alveolar pressure to correct which is best accomplished by increasing the IPAP and EPAP in tandem which forces fluid out of the alveoli by an increase in the overall mean alveolar pressure [9,10].  This increase in pressures must done slowly to balance the need for increased pressures against patient comfort and the limit of recruitable alveoli. Persistent need for EPAP pressures 10-12cm H20 should push management toward intubation [10].

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Expert Commentary

Thank you for the opportunity to review this helpful post. As you mention, non-invasive positive pressure ventilation (NPPV) is a potentially life-saving supportive therapy for patients with acute respiratory failure. Emergency Medicine providers should be familiar with when and how to use this important tool.

 If I were to highlight just one thing in your post, it would be your suggestion to “start monitoring.” This should be in bold and in 30-point font.

Attentive bedside monitoring of patients recently placed on NPPV matters exponentially more than any other aspect of therapy.

NPPV can decrease work of breathing, improve oxygenation, improve alveolar ventilation, and counteract auto-PEEP. All of these can and should be monitored at the bedside as the pressure requirements to achieve these goals will differ with each patient depending on the mechanics of their respiratory system and the severity of their disease. Close bedside monitoring is also essential to determine if a patient is failing a trial of NPPV and requires invasive mechanical ventilation. When returning to the room, you should be asking yourself the following: Has my patient’s work of breathing improved? Is my patient still hypoxemic? Is their respiratory acidosis better? Are they having difficulty with secretions? How is their mental status? Many studies show that delaying intubation, when ultimately necessary, worsens outcomes so it is critical to recognize a failing patient early and take control of the situation. I think it’s often helpful to set a clear time limit with NPPV, for instance “I am going to trial NPPV in this patient with acute decompensated heart failure (ADHF). If his work of breathing and RR remain high in 20 minutes, we will move towards intubation.” In general, if you place a patient on NPPV in the emergency department (ED), you should plan to return to their bedside frequently over the next 45 minutes. Make this part of your practice.

A few points on terminology since it’s confusing:

• Expiratory positive airway pressure (EPAP) on NPPV is the same as positive end-expiratory pressure (PEEP) when using invasive mechanical ventilation.
• Continuous positive airway pressure (CPAP): an NPPV mode where the machine delivers a continuous level of airway pressure (e.g., on CPAP 5, the machine will continuously deliver 5 cmH20 during inspiration and expiration). Breaths in this mode are all patient triggered (an apneic patient will remain apneic on CPAP) and not supported with any additional pressure support.
• Bilevel positive airway pressure (BPAP): an NPPV mode where you set an EPAP and an inspiratory positive airway pressure (IPAP). Breaths in this mode are patient-triggered (an apneic patient placed on BPAP will remain apneic unless your machine has a backup rate), pressure-targeted (the machine delivers the set IPAP with each patient-triggered breath), and flow-cycled (the IPAP is delivered until the machine senses a set % decrease in patient inspiratory flow at which point the pressure drops back to EPAP and the patient passively exhales). As this is a pressure mode, you do not directly control the tidal volume; instead it is determined by patient effort, respiratory system mechanics, and the difference between IPAP and EPAP (also known as the driving pressure or pressure support). A higher driving pressure (a bigger difference between IPAP and EPAP) will produce a bigger tidal volume.
• BiPAP and BIPAP: these are two proprietary modes of BPAP (the first by Respironics and the second by Drager). It’s unnecessarily confusing, I know, but just be aware that BiPAP and BIPAP are brand names, BPAP is the generic term which you should be using.
• On BPAP, airway pressure cycles from the set EPAP to the set IPAP (e.g., on BPAP 15/5, the pressure will cycle from 5 cmH20 to 15 cmH20 with each breath). On invasive mechanical ventilation in the pressure control mode, you don’t set an IPAP but rather a desired level of pressure support (PS). This is the pressure above PEEP. So on PS 15/5, the pressure will cycle from 5 cmH20 to 20 cmH20 (15 cmH20 above PEEP). In other words, BPAP 15/5 will generate the same pressures as PS 10/5.

 Some basic suggestions on settings:

• EPAP and IPAP settings can be adjusted in increments of 2-3 q 5 minutes as needed
• Titrate EPAP to achieve the desired O2 saturation (aim for >88% in COPD pts who are chronic CO2 retainers).
•  As noted, the level of PS is defined as IPAP-EPAP; increased IPAP-EPAP=increased tidal volume/increased ventilation.
• Begin with IPAP 5 cmH2O above EPAP (to provide 5 cmH2O of PS); increase IPAP-EPAP as needed, titrated to lessen the RR, lessen the visible work of breathing, and decrease PCO2 in hypercapnic pts 
• Remember that whenever you increase EPAP you have to increase IPAP by a similar amount to maintain the same level of PS (e.g., if inadequate oxygenation: change 10/5 to 13/8 to keep a PS of 5 cmH20).
•  In general, EPAP should not exceed 8-10 cmH2O and IPAP not exceed 20 cmH2O (this level of support should make you strongly consider intubation).
•  Titrate FiO2 down to ≤60% as long as adequate O2 saturation is maintained.
•  EPAP/PEEP: In addition to decreasing preload and reducing airway collapse at end-expiration as you mention, EPAP/PEEP also counteracts the effects of auto-PEEP (which helps decrease work of breathing in severe COPD/asthma) and decreases left ventricular afterload.

Just to be clear, NPPV does not a have strong evidence base in all forms of pulmonary edema, only hydrostatic/cardiogenic pulmonary edema (ADHF). In ADHF, NPPV (especially the EPAP part) works as an LV assist device by dropping LV preload and decreasing LV afterload. Whether you place a patient in ADHF on CPAP or BPAP doesn’t seem to matter much. This was best studied in a 2008 NEJM trial that did not show any clear benefit to BPAP vs CPAP (although both were better than standard O2). It is important to remember that the use of NPPV/EPAP may cause clinical deterioration in patients with right ventricular failure. EPAP increases RV afterload and drops RV preload so close bedside monitoring is essential if using NPPV in patients with RV failure.

ARDS is also a pulmonary edema syndrome (edema in ARDS is caused by disruption of the alveolar epithelial/endothelial barrier) but the evidence for NPPV is much weaker than in ADHF. Based on some recent trials, many of us are moving towards high-flow nasal cannula in this setting rather than NPPV (reviewed in detail here).

 A small semantic point: Throughout your review, you mention monitoring “compliance.” Generally, “compliance” denotes a patient’s willingness to follow treatment recommendations. “Non-compliance” tends to be a negative term; a patient knows what they should do but chooses to do otherwise. What you are assessing when using NPPV in the ED is not “compliance” but “tolerance.” In 99% of cases, the factors that limit use of NPPV in acutely ill patients in the ED are not within a patient’s control: fear, anxiety, delirium, vomiting, feeling like they are unable to breathe or get enough air, etc.

Talk with RT and your program leadership to find a time to trial NPPV. Clinicians who use NPPV should know what a high EPAP or driving pressure feels like so you can better coach your patients through what they are going to experience when starting therapy.

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James "Mac" Walter

Instructor of Medicine, Pulmonary and Critical Care

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How to cite this post

[Peer-Reviewed, Web Publication]   McCauley M, Sanders S (2018, July 16 ). Non-invasive positive pressure ventilation in the emergency department.  [NUEM Blog. Expert Commentary by Walter J]. Retrieved from http://www.nuemblog.com/blog/NIPPV

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References

1. Cabrini L, Landoni G, Oriani A, et al. Noninvasive ventilation and survival in acute care settings: A comprehensive systematic review and metaanalysis of randomized controlled trials. Crit Care Med 20 2015 Apr;43(4):880-8
2. Carlson JN, Wang HE. Noninvasive Airway Management. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016
3. Confalonieri  M, Potena  A, Carbone  G, Porta  RD, Tolley  EA, Umberto Meduri G. Acute respiratory failure in patients with severe community acquired pneumonia. A prospective randomized evaluation of noninvasive ventilation. Am J Respir Crit Care Med. 1999;160(5 Pt 1):1585–1591
4.  Keenan SP Mehta S. Noninvasive ventilation for patients presenting with acute respiratory failure: the randomized controlled trials. Respir Care 2009;54:116–26
5.  Kelly CR, Higgins AR, Chandra S. Noninvasive positive-pressure ventilation. N Engl J Med 2015;372:e30-e30
6.  Liesching T, Kwok H, Hill NS. Acute applications of noninvasive positive pressure ventilation. Chest 2003; 124: 699–713.
7. LIGHTOWLER JVJ, ELLIOTT MWPredicting the outcome from NIV for acute exacerbations of COPD Thorax 2000;55:815-816
8. Lim WJ, Mohammed Akram R, Carson KV, Mysore S, Labiszewski NA, Wedzicha JA, Rowe BH, Smith BJ. Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane Database of Systematic Reviews 2012, Issue 12.
9.  Vital FM, Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary edema. Cochrane Database Systematic Reviews  2013 Issue 5
10. Wright BJ, Slesinger TL. Noninvasive Positive Pressure Ventilation. In: Farcy DA, Chiu WC, Marshall JP, Osborn TM. eds. Critical Care Emergency Medicine, 2e New York, NY: McGraw-Hill