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How to obtain it, what “normal” looks like, and what you’re screening for... The right ventricular outflow tract (RVOT) view is a cornerstone of fetal cardiac screening because it shows the right ventricle connecting to the main pulmonary artery, the pulmonic valve, and often the pulmonary artery bifurcation—structures that are essential for recognizing conotruncal anomalies and outflow obstruction. ISUOG and ASE both emphasize routine assessment of outflow-tract views, including RVOT. Why the RVOT view matters A clean RVOT view helps you evaluate:
This is one of the key views used to screen for:
 RVOT acquisition from the 4-chamber view (sweep technique) Step-by-step (4CH → RVOT):
RVOT acquisition from the short-axis (SAX) view This approach is great when your 4CH sweep keeps “missing” the outflow, or when you want a more reproducible pathway. Step-by-step (SAX → RVOT):
 LPA or Ductus? That is the question... When you’re evaluating the pulmonary artery branches in the short-axis (SAX) view, one of the most common moments of hesitation is this: “Am I looking at the left pulmonary artery… or did I just slide into the ductus?” It’s a fair question—and a very normal one. The key is to stop thinking of these as two identical tubes and start thinking about where they go and how they behave. Start with anatomy and direction - From the main pulmonary artery: The left pulmonary artery (LPA) branches laterally toward the left lung. It stays within the pulmonary circulation and does not head straight into a systemic vessel. The ductus arteriosus courses posteriorly and inferiorly, connecting the pulmonary artery to the descending aorta. It has a longer, more continuous “run” compared to a branch PA. If the vessel looks like it’s heading off to the lung and disappearing laterally, you’re likely following the LPA. If it looks like it’s traveling away from the heart in a smooth arc toward the descending aorta, that’s the ductus. Use size and appearance as supporting clues The ductus arteriosus is typically larger and more dominant than the branch pulmonary arteries in the fetus. The LPA is smaller and more branch-like, especially earlier in gestation. Size alone isn’t diagnostic—but it helps reinforce what direction and continuity are telling you. Sweep intentionally, not randomly A common pitfall is overshooting the branch level. If you’re unsure:
Small, controlled movements keep you oriented. 💡 If it connects to the descending aorta, it’s the ductus. If it heads toward the lung and branches, it’s the LPA. Once you start following the vessel’s destination—not just its shape—this distinction becomes much easier and far more intuitive. What “normal RVOT” should look like (how it feels when you’re in the right place) When you’re truly in the RVOT, things start to line up and make sense. You should see the pulmonary valve opening easily, with thin, mobile leaflets—nothing stiff, domed, or restricted. It should look like it wants to open. The main pulmonary artery should come directly off the right ventricle and course anteriorly in front of the aorta in this plane. If it looks like it’s sneaking behind or doesn’t clearly connect to the RV, pause and reassess your angle. And here’s the reassurance check: when you capture the LVOT as well, the aorta and pulmonary artery should cross right at their origins. That normal crossover is one of the quickest ways to confirm you’re looking at the right outflow—and not mixing up vessels. When all three of those pieces fall into place, you can be confident you’re truly in the RVOT.  Color Doppler: confirm patency and direction (without killing your frame rate) Once your grayscale RVOT looks solid, color Doppler is your reality check—but this is one of those moments where less is more. Keep the color box small and focused right over the pulmonary valve and proximal main pulmonary artery. A big box might feel safer, but it will tank your frame rate and make everything harder to interpret. Set your color scale that matches fetal flow. Typically >50cm/s is needed for RVOT flow. However when evaluating the septum, a lower velocity scale is helpful. You’re not looking for adult-level velocities here—too high and you’ll miss important flow detail. Now confirm the essentials:
You’re simply confirming that blood is leaving the right ventricle the way it should. And remember, outflow tract views and great vessel views with color Doppler aren’t optional. They’re a routine and expected part of fetal cardiac screening and full fetal echocardiography documentation.  Pulmonary Artery, when size really matters... When comparing the pulmonary artery (PA) and aorta (AO) in the fetus, it’s important to remember that the PA is normally equal to or slightly larger than the aorta. This makes sense physiologically—the right ventricle is the dominant ventricle in fetal circulation, and most of the cardiac output is directed through the pulmonary artery and ductus arteriosus. If the PA appears significantly smaller than the AO, that should raise concern for RVOT obstruction, pulmonary stenosis, or conotruncal abnormalities. On the other hand, a markedly enlarged PA relative to the aorta can suggest increased pulmonary flow or downstream obstruction. Size comparisons are never interpreted in isolation, but they provide an important visual clue when evaluating fetal outflow tracts. Common pitfalls (and quick fixes)
If you can demonstrate: RV → pulmonary valve → main PA (± bifurcation), you have RVOT. Then pair it with LVOT to confirm normal crossover (one of the quickest sanity checks in fetal outflow evaluation)
Curious about learning fetal echocardiography - our Fetal Echo Cross Training Course can get you there. We have a course option that might be just what you're looking for. Want to be sure it’s the right fit? The Fetal Echo Preview Access Pass lets you experience how we teach fetal cardiac imaging—before making a bigger investment. 👉 Try the Fetal Echo Preview Pass now or join us for upcoming Intro to Fetal Echo Hands On Training Workshop! Keep Scanning! - Lara Williams, BS, ACS, RCCS, RDCS, RVT, RDMS, FASE
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Why it matters, how to obtain it, and what it tells you... The left ventricular outflow tract (LVOT) view is one of the most critical components of a complete fetal echocardiogram. While it may look deceptively simple, this view plays a major role in confirming normal ventriculo-arterial connections, evaluating aortic valve anatomy and flow, and screening for some of the most serious congenital heart defects. The LVOT view answers the question “Is blood leaving the left ventricle the right way?” Why the LVOT View Is So Important The LVOT view allows the sonographer to:
 Where to Start: The Four-Chamber View Every good LVOT view begins with a true four-chamber view. Before sweeping:
How to Obtain the LVOT View From the four-chamber view:
What does a Diagnostic LVOT View look like? A technically adequate, normal LVOT view includes:
 Using Color Doppler in the LVOT Once grayscale anatomy is optimized, color Doppler is essential. Color helps you:
 Common Pitfalls to Avoid Common challenges include:
The Big Picture The LVOT view is more than a checkbox—this imaging view allows for physiology and alignment assessment that connects structure with flow. When mastered, it becomes one of the most satisfying views in fetal echocardiography and a powerful tool for early diagnosis. For sonographers learning fetal echo or cross-training into fetal cardiac imaging, developing confidence with the LVOT view is a major milestone. Curious about learning fetal echocardiography - our Fetal Echo Cross Training Course can get you there. We have a course option that might be just what you're looking for. Want to be sure it’s the right fit? The Fetal Echo Preview Access Pass lets you experience how we teach fetal cardiac imaging—before making a bigger investment. 👉 Try the Fetal Echo Preview Pass Now! Keep Scanning! - Lara Williams, BS, ACS, RCCS, RDCS, RVT, RDMS, FASE  Diastology can often be confusing, as there have many updates to the standards and guidelines regarding how to assess and grade left ventricular diastology in the past few years. So let's dig in to how to assess this and the echocardiographer's role in evaluating diastology based on the updated 2016 ASE Guidelines. So as cardiac sonographers, we should all know the basics... E/A reversal = Diastolic Dysfunction, but there is a little more to it than that. If you're not fully evaluating diastology with additional measures, you're probably missing some positive cases. Also the Intersocietal Accreditation Commission now includes reporting of left ventricular diastolic function as a requirement for echocardiography accreditation.  What exactly is diastolic dysfunction? This is a decrease in left ventricular compliance during diastole. While the ejection fraction and left ventricular systolic function are needless to say, pretty important, the diastolic function of the heart is important too. If the heart does not rest properly during diastole, then it cannot fill with the right amount of blood volume needed and eventually this can lead to heart failure and significant clinical implications. So it's important to know the left atrial pressures and end diastolic left ventricular pressures in order to determine the level of severity of the diastolic dysfunction. The updated guidelines break it down like this: Grade 0 = Normal Grade 1 = Impaired Relaxation/Diastolic Dysfunction Grade 2 = Pseudonormalization Grade 3 = Restrictive Pathophysiology So how do we get to the diagnosis? Based on the updated standards from the ASE, determination of normal vs diastolic dysfunction is evaluated initially, based on the patient's EF. If a patient has a normal ejection fraction then the algorithm looks at four components to determine whether or not the patient has a degree of diastolic dysfunction: 1. Average E/e’ > 14 2. e' velocity -Septal e’ velocity < 7 cm/s -Lateral e’ velocity <10 cm/s 3.TR velocity > 2.8 m/s 4. LA volume index >34ml/m2 If <50% are positive, the patient is considered normal. If >50% are positive, the patient has a degree of diastolic dysfunction. If only 50% are positive, then we are unable to determine whether the patient has diastolic dysfunction. If the patient has a compromised ejection fraction, then we can assume that there is a degree of diastolic dysfunction and can grade it based on the E/A ratio. When the mitral inflow pattern shows an E/A ratio <0.8 along with a peak E velocity of <50cm/sec, then the mean LAP is either normal or low and this is considered a Grade 1. When the mitral inflow pattern shows an E/A ratio of >2, the mean LAP is elevated, consistent with Grade 3 diastolic dysfunction. Keep in mind patients with young or athletic patients may show this ratio in the setting of normal diastolic function. Also, patients in atrial fibrillation may exhibit a reduced or loss of the mitral A wave and may also produce similar findings. For patients with reduced EF's that do not meet one of those parameters and the mitral inflow shows an E/A Ratio >0.8 AND the peak E velocity is >50 cm/sec OR E/A Ratio >8 but <2, then other parameters are required for determination of diastolic dysfunction. 1. Average E/e’ Ratio - average E/e’ ratio >14 2. TR Velocity - peak jet velocity >2.8 m/sec 3. LA Volume Index - >34 mL/m2 If 2 of 3 are negative, the patient is considered to have Grade 1 diastolic dysfunction, where if 2 of 3 are positive, then this is considered Grade 2. So, are you confused yet? Let's look at the grading parameters a little closer. GRADE 0 - NORMAL DIASTOLOGYThis means that left atrial pressures (LAP) are normal and the diastolic function is not impaired. The left ventricle relaxes normally throughout diastole and allows for complete diastolic filling. The E/A ratio in a normal setting, is between 1 and 2. This gradually reduces with age and E/A ratio >0.75 may be considered normal above 75 years.  GRADE 1 - IMPAIRED RELAXATION/DIASTOLIC DYSFUNCTIONPatients that do not have a NORMAL EF, will have a degree of diastolic dysfunction and are evaluated based on filling pressures of the left atrium. Left atrial pressures can be somewhat normal in a patient with Grade 1 diastolic dysfunction, but will increased as this progresses. Patients with Grade 1 diastolic dysfunction will have reduced e' velocities and prolonged deceleration time.  GRADE 2 - PSEUDONORMALIZATIONOne of the biggest factors that our role as sonographers requires, is knowing your patient history. This will often help you know whether or not you're dealing with a normal waveform or pseudonormalization. Granted there are some other key factors but the most obvious is whether or not the patient has previously been diagnosed with diastolic dysfunction. If they have previously had reversal of the E/A waveform and now have a normal waveform pattern, this is a pretty good indicator that the patient is in pseudonormalization. Also, keep in mind some of the other factors associated with increased left atrial pressures, such as blunting or changes to the pulmonary venous waveform, as well as reduced e' velocities. When pseudonormalization is present, the valsalva maneuver can assist to "unload" the ventricle and to reduce filling pressures, causing the E/A reversal to be unmasked.  GRADE 3 - RESTRICTIVE FILLING PATTERNGrade 3 diastolic dysfunction involves increased left atrial pressures and increased end diastolic left ventricular pressure. This may result in reversal of the pulmonary venous waveform and is often seen with the presence of left atrial enlargement and left ventricular hypertrophy.  ECHO DIASTOLOGY GRADING ANALYSIS TOOLS!The newly updated algorithm for determining diastology and left atrial pressures can be a little overwhelming and difficult to follow, but we make it easy with our Echocardiography Analysis Tools which include our exclusive LV Diastology Assessment Tool! Quickly and easily determine and grade the diastology based on the updated ASE guidelines. Also there are many other parameters that affect diastology and the application of the diagnostic criteria, such as age, athletic hearts and other factors. Learn and review these additional factors and an in depth study of diastolic dysfunction in our MASTERING LV DIASTOLOGY CME COURSE!
REFERENCE: ASE/EACVI GUIDELINES AND STANDARDS Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging; Nagueh et al
Please note: allaboutultrasound.com and iheartecho.com are not endorsed by or affiliated with the American Society of Echocardiography  Mastering Echocardiography can be tough, especially when it comes to complex processes like Constrictive Pericarditis. Patients with Constrictive Pericarditis do not present for typical pericarditis symptoms. Instead, they present with symptoms of heart failure and so this can often be a challenge for even very skilled sonographers to identify the subtle differences between Restrictive Cardiomyopathy and Constrictive Pericarditis. These two disease processes can appear very similar on echocardiography. However, there are a few things that clue us into the correct diagnosis.  Constrictive Pericarditis is seen with a fibrotic, thickened pericardium, which insulates the ventricle and constricts the ventricle from fully relaxing during diastole. Whereas, Restrictive Cardiomyopathy results in a thickened myocardium, which inhibits the ability of the ventricle to relax and also results in abnormal diastolic function. However, that's where the similarities end. First of all, we need to evaluate for interdependence of the ventricles. But what does that mean? Ventricular interdependence is when there is a respiratory ventricular septal shift. This then leads to an increase in the volume of one ventricle associated with a decreased volume in the opposite ventricle. This can be tricky to diagnose, so it takes a pretty detailed echo exam and a keen eye of the sonographer and physician.  Secondly, when evaluating for constriction, we will need to look at respiratory changes to the Doppler waveform patterns. The respiratory changes in the Mitral inflow pattern will show a variation of greater than 15% when constriction is present. Whereas, with restriction, this waveform pattern will show a restrictive filling pattern with an E/A ratio >2.0 and deceleration time <160ms.  Another key factor in determining constriction vs. restriction is the E/e' ratio and diastolic function. Remember that both disease processes will have a degree of diastolic dysfunction. Normal left ventricular function will typically show a lateral e’ greater than septal/medial e' velocities, because the septal wall is somewhat restricted and the lateral wall is more free to move. However, with constriction the pericardium is insulating the ventricular movements and does not allow for full relaxation and movement of the lateral wall. This results in mitral annulus reversus, which is a decreased lateral e' velocity and compensatory increase in tissue velocities in the septal/medial annulus. Restrictive patterns in tissue velocities will show an overall decrease in both the lateral and septal e' velocities.  Additionally, with constriction, this will result in expiratory hepatic vein reversal. But why does this occur? Remember that air moves from areas of high pressure to low pressure, which allows for air flow into the lungs. During expiration, the volume of air (and the pressure) of the thoracic cavity decreases, causing the intrapulmonary pressure to rise above the atmospheric pressure. However, with constriction, the pericardium is insulating the intracardiac chambers and this keeps them from tracking normally with intrapulmonary pressures. Remember the pulmonary artery and aorta are OUTSIDE of the pericardium. So with constriction the thorax pressure and the pulmonary venous pressure will drop, but there are phasic filling differences within the heart, because the gradient to fill the left side of the heart is decreased. The heart is no longer able to push outward against the pericardium, so the pressure is forced inward into the cardiac chambers. So during expiration, the pressure in the right atrium causes flow reversal in the hepatic veins. Whereas, with chronic late stages of restriction, there is an inspiratory reversal during diastole, because there is no shifting of septum and the right heart cannot accommodate increased flow which results from chronic diastolic dysfunction and this causes hepatic vein reversal. While diagnosing Constrictive Pericarditis on echocardiography can certainly be a challenge, it can be done with confidence. Paying close attention to the details and recognizing when your patient with heart failure symptoms might actually be more than meets the eye, can help to make the correct diagnosis and ensure adequate treatment for your patient. Want more information on the differences between Constrictive Pericarditis and Restrictive Cardiomyopathy, including Strain Imaging methods? See our E-Learning Course Mastering Constrictive Pericarditis and earn 1 SDMS CME credit. REFERENCES
In recent medical news, an article was posted regarding a research trial involving ultrasound micro-bubbles and cavitation to repair myocardial infarctions in mice. This amazing research opens up so many possibilities for human MI tissue repair and proves that medical ultrasound is beneficial for so much more than it's current use. See the full article at the following link:
http://www.news-medical.net/news/20130221/Microbubble-ultrasound-method-improves-cardiac-output-after-heart-attack.aspx Ultrasound Accreditation and/or sonographer credentialing requirements are already in effect in many states and soon will be required for reimbursement of exams. Is your ultrasound lab accredited? If not, are the sonographers in your department registered? How is your lab preparing for the upcoming accreditation requirements?
How in depth does your echocardiography department go to classify the grade of LV diastolic dysfunction? Do you perform tissue Doppler? Do you grade by E/e' ratio? Do you sample tissue Doppler at only the lateral wall or also include the septal wall?  What is the method of diagnosis for this patient? How would you as the sonographer prove the findings seen below? What is the prognosis for this patient?
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