Right Ventricular Ultrasound-Qualitative and Quantitative Assessments

Authors: Eduard Krishtopaytis MD, Anissa Johnson MD, Sushil Pant MD, Vi Dinh MD.

When you’re using POCUS to assess right ventricular (RV) or right heart function, chances are you’re dealing with a critically ill patient—someone with pulmonary embolism, pulmonary hypertension, right-sided heart failure, or even a right-sided myocardial infarction. In these high-stakes situations, you don’t have the luxury of waiting for a formal cardiology report. You need answers fast. That’s why it’s crucial for providers to understand RV physiology, evaluate RV pathology, and perform a reliable bedside RV assessment.

However, evaluating the Right Heart and RV with POCUS and echocardiography isn’t straightforward. Unlike the left ventricle (LV), which has a simple circular shape, the RV is a crescentic, complex structure that requires multiple views for proper assessment. Its retrosternal position makes image acquisition challenging, and while many parameters can be measured, there isn’t a single gold-standard value that defines RV function. Moreover, no universally accepted algorithm exists for RV assessment, adding to the complexity. However, in this guide, we’ll show you a basic way to assess the RV using step by step qualitative and quantitative methods.

After reading this post, you’ll learn:

• How to obtain optimal sonographic windows specific to the RV.
• Both Qualitative AND Quantitative RV measurements—their physiological basis, how to acquire them, and how to interpret the findings.
• Common pitfalls and challenges in RV assessment and how to overcome them.

By the end of this review, you’ll have a clear, practical approach to evaluating RV function at the bedside—when it matters most.

RV Anatomy and Echo Views

The most common views to assess for right ventricular function are the parasternal long axis, parasternal short axis (mid-papillary level), and apical 4 chamber view. The subxiphoid view can also be performed with the parasternal or apical views cannot be obtained. For a complete tutorial on all of the cardiac ultrasound views, just click here.

Here is a brief overview of these views.

Parasternal Long-Axis (PSLA) View

The heart lies in an oblique orientation, with the right ventricle anterior to the left ventricle. The Parasternal Long Axis View (PSLA) is used to assess RV size compared to the LV size.

Parasternal Short-Axis (PSSA) View-Mid Papillary Level

The parasternal short-axis view (PSSA) gives a cross-section of the heart. The PSSA view should be obtained at the level of the papillary muscles to look for RV to LV ratio as well as to the assess the D-Sign.

Parasternal Short-Axis (PSSA) View-Aortic Valve Level

The parasternal short-axis view (PSSA) view at the aortic valve level is another view you can assess for Tricuspid Regurgitation (TR) as well as measure the Right Ventricular Outflow Tract Velocity Time Integral (RVOT VTI).

Apical 4 Chamber (A4C) View

The apical four-chamber view can be used to measure Tricuspid Annular Plane Systolic Excursion (TAPSE) as well as Tricuspid Regurgitation (TR).

Subxiphoid (Subcostal) View

The subxiphoid view can be used to look for RV dilation as well as to measure the RV Free Wall Thickness. This will help differentiate between chronic vs acute elevations in right heart pressures.

Inferior Vena Cava (IVC) View

The IVC view will be necessary to estimate right atrial pressures (RAP) and central venous pressure (CVP).

Here is a quick summary on how you can use the views for each of the assessments we will be going over.

Parasternal Long Axis	RV/LV Ratio TR Velocity/RVSP (Inflow View) RVOT VTI (Outflow View)
Parasternal Short Axis	D Sign TR Velocity/RVSP RVOT VTI RVOT Acceleration Time (60/60 Sign) PVR
Apical 4 Chamber	McConnell’s Sign TR Velocity/RVSP • TAPSE • S’ Wave • TR Peak Velocity • 60/60 Sign – Part 2 (TR velocity) • RV Dilation (RV/LV Ratio) • Right Heart Thrombus (if visible) • PVR (complete with TR velocity)
Subxiphoid View	RV/LV Ratio
IVC View	CVP Estimation RVSP

Qualitative Approach to RV Assessment

When first performing RV assessments, it is best to learn qualitative signs as they are easy to learn and incorporate into your practice right away!

RV to LV Ratio

The RV to LV ratio is one of the most simple ways to qualitatively assess if RV dysfunction is present. The RV is normally smaller than the LV and as it enlarges the RV to LV ratio will increase.

POCUS 101 Tip: An easy rule of thumb is to qualitatively see if the RV is equal to or larger than the RV, if so then there is likely RV dilation.

To assess the RV to LV ratio, you can use the Parasternal Long Axis, Parasternal Short Axis, Apical 4-chamber views, and Subxiphoid views. All of these views work because you can view BOTH the RV and LV simultaneously. You can use a simple eyeball method to see if the RV is as large or larger than the LV!

Here are some examples of enlarged RV to LV ratios:

To precisely calculate the RV ratio, simply divide the RV distance by the LV distance use the following steps

Step 1: Obtain an Apical 4-Chamber View

Step 2: Freeze the image in end-diastole (when the RV is largest, just before tricuspid valve closure).

Step 3: Visually compare the size of the RV to the LV to get an estimate. For a specific ratio, divide the measurement of the RV diameter by the measurement of the LV diameter at the base of the heart (see corresponding location seen below). Then, simply divide the RV Diameter/LV Diameter to get the ratio!

Here are some easy numbers to remember to interpret the RV to LV ratio:

• RV/LV Ratio of 0.67:1 to 1:1 is considered mildly dilated
• RV/LV Ratio of 1:1 to 1.5:1 is considered moderately dilated
• RV/LV Ratio of >1.5:1 is considered severely dilated

In addition, you can measure specific areas of the right ventricle with the following cutoffs:

POCUS 101 Extras:

RV dilation has: sensitivity of 50%, specificity of 98%, a positive predictive value of 88%, and a negative predictive value of 88% for diagnosis of pulmonary embolism (Dresden, et al).

Assessing the RV wall thickness helps differentiate the acute vs chronic enlargement of the RV cavity size. A RV wall thickness >5 mm in the end-diastolic phase is considered thickened RV and associated with chronically increased RV pressures (Rudski, et al).

Increased RV/LV diameter ratio may be associated with increased risk of short-term death in patients with acute pulmonary embolism (Cimini, et al).

D Sign

The “D Sign” is an ultrasound/echo finding that shows the left ventricle in the Parasternal Short Axis View (Mid Papillary Level) as a D-shaped structure. It is a result of right ventricular overload causing a shift of the septum towards the left side of the heart. The “D-sign” can be the result of either right ventricular Pressure and/or Volume overload.

POCUS 101 Tip: An easy rule of thumb is to qualitatively see if the an enlarged RV is pushing against the septum to cause the LV to appear as a “D shape.”

Here are some examples of the D Sign on Ultrasound/Echocardiography:

The Eccentricity Index (EI) is an echocardiographic measurement of the left ventricle that can quantify the amount of right ventricular strain and overload affecting the left ventricle. It is described by Ryan et al and is calculated by taking two measurements of the left ventricular cavity.

The first measurement (D1) is taken perpendicular to the septum, and the second measurement (D2) is taken parallel to the septum. The eccentricity index is then simply calculated by the following equation: Eccentricity Index (EI) = D2/D1.

Here is how to interpret the Eccentricity Index:

• EI < 1: Normal
• EI > 1: Right Ventricular Overload with resulting “D Sign”

POCUS 101 Extras: 

“D-sign” is considered highly specific but low in sensitivity for a PE. One meta-analysis noted a sensitivity of 53% and a specificity of 83%.

In right ventricular pressure overload, patients will have an EI of > 1.0 (with D Sign) in BOTH end-systole and end-diastole, while in volume overload patients will have an EI > 1.0 (with D Sign) during end-diastole, and a normal eccentricity index (<1) during end-systole.

Is present in Pulmonary Embolism, Pulmonary Hypertension, Chronic Right Heart Failure with Hypertrophy, Left-sided heart failure, Acute Respiratory Distress Syndrome (ARDS).

McConnell’s Sign

McConnell’s Sign occurs when the lateral wall of the right ventricle does not move (akinesia) or has decreased movement (hypokinesia) while the apical wall has hyperdynamic contraction.

This can be seen by obtaining the Apical 4-Chamber View:

Physiology   

• The presence of this sign is indicative of acute right ventricular strain, which manifests because of the increased pressure present in the right heart inhibiting the lateral wall’s contraction. 
• The apex of the right ventricle is believed to be “tethered” to the left ventricle, which is why this portion of the right heart continues to contract despite the increased resistance.
• A pulmonary perfusion defect of at least 25% (moderate degree) is required for McConnell’s sign to be demonstrated

POCUS 101 Extras: 

RV apex is only “contracting“ due to preserved LV function. 

77% sensitivity and 94% specificity for diagnosing acute pulmonary embolism, a positive predictive value of 71% and a negative predictive value of 96%. It can also be seen in RV infarct or severe pulmonary hypertension (Foley, et al).

Right Heart Thrombus

The presence of a clot or thrombus in the right atrium or ventricle is one of the most direct qualitative signs that a patient has a clot in transit to the pulmonary arteries, causing a pulmonary embolism. This can directly be seen best in the Apical 4 chamber view or Subxiphoid views as an echogenic mobile structure in either the right atrium or the right ventricle.

POCUS 101 Extras:

Multiple studies demonstrated a strong association between Right Atrial or Right ventricular thrombus with increased risk of mortality.

In patients with a diagnosed pulmonary embolism, a right heart thrombus is uncommon, ranging from 3.6% to 23.3% of cases (but considered to be ‘very specific’ for a PE (although no % calculated), (Jammal, et al).

IVC Collapsibility (CVP Estimate)

IVC measurement and CVP estimation are key parts of RV echo assessment because they provide insight into right heart filling pressures and volume status. This context is crucial when interpreting RVSP, assessing for elevated pulmonary vascular resistance (PVR), or identifying signs like the 60/60 sign which we will go over in the Quantitative section of the post.

Here is a simplified and practical table you can use to interpret your IVC findings.

IVC Size	IVC Collapsibility	Interpretation (CVP)
< 1.5cm	>50% collapsibility	0-5 mm Hg (Low CVP)
1.5-2.5cm	>50% collapsibility	6-10 mm Hg
1.5-2.5cm	<50% collapsibility	11-15 mm Hg
>2.5cm	<50% collapsibility	16-20 mm Hg (High CVP)

The caveat about IVC measurements is that it just gives you a static measurement to estimate the central venous pressure. So all of the limitations of using CVP will also pertain to IVC measurements.

POCUS 101 Extras

IVC diameter and the presence of inspiratory collapse depend on the interplay of internal distending pressure and external compressive pressure. The external compressive pressure is relatively static and the internal distending pressure is very dynamic and is a result of the combination of factors affecting venous return, right heart function, and intrathoracic pressure relative to intra-abdominal pressures. IVC diameter and collapsibility index have been used in estimating the CVP which may be elevated in pulmonary embolism (Fields, et al). 

Although no studies have used IVC collapsibility in pulmonary embolism, multiple studies have reported a sensitivity of 47% to 91% and a specificity of 77% to 94% IVC diameter and IVC collapsibility in estimating CVP (Prekker, et al; Nagev, et al; Brennan, et al; Cimini, et al). Nagdev et al reported a sensitivity of 90.9% and specificity of 94.1% of bedside POCUS IVC collapsibility index >50% as a predictor of CVP < 8 mm Hg.  Prekker et al reported that a maximal IVC diameter < 2 cm had a sensitivity of 85% and specificity of 81% in predicting a CVP <10 mmHg. Brennan et al reported a maximal IVC size cutoff of 2 cm had a sensitivity of 73% and a specificity of 85% for predicting RAP greater than 10 mm Hg.

Quantitative Approach to RV Assessment

Quantitative assessments of the RV using echocardiography will require more practice and advanced modalities, such as M-Mode, Pulse Wave, Continuous Wave, and Tissue Doppler. However, with some practice, these measurements will give you a much more accurate and detailed assessment of RV function.

Right Ventricular Free Wall Thickness

One of the easiest quantitative RV assessments is measuring the Right Ventricular Free Wall Thickness.

The thickness of the right ventricular wall, in conjunction with the presence of other signs of right heart strain seen on echocardiography, can help determine the chronicity. The lateral wall of the right ventricle, measuring more than 5mm, indicates that the right heart strain is chronic.

Step-by-Step Guide for RV Free Wall Thickness Measurement:

POCUS 101 Extras:

The wall of the right ventricle increases in thickness due to ‘adaptive remodeling’ – a compensatory process the heart undertakes in order to maintain the right ventricle’s stroke volume as pressure within the right ventricle rises (Bryce, et al).

Right ventricular hypertrophy can be seen in chronic thromboembolic pulmonary hypertension which can occur after an individual suffers from multiple acute pulmonary emboli.

Chronic lung disease is most commonly associated with right ventricular hypertrophy. However, this can also be seen in left heart failure, pulmonary hypertension, and interstitial lung disease.

Tricuspid Annular Plane Systolic Excursion (TAPSE)

Tricuspid annular plane systolic excursion (TAPSE) is a type of regional assessment of RV systolic function. It measures RV longitudinal function by measuring the distance of systolic excursion of the RV annular segment along its longitudinal plane. Prior studies have shown that TAPSE correlates with RV Ejection Fraction.

Step-by-Step Guide for TAPSE Measurement:

*Mode Required: M-Mode

TAPSE Interpretation

Normal TAPSE: A TAPSE value greater than 16 mm typically indicates normal right ventricular function.

Reduced TAPSE: A TAPSE value less than 16 mm suggests possible right ventricular systolic dysfunction or impaired right ventricular function. This can be seen in pulmonary hypertension, pulmonary embolism, with right ventricular strain, and right ventricular myocardial infarction (MI). (Rudski et al.)

POCUS 101 Extras:

 

Physiology behind TAPSE – The Right ventricle consists of 2 layers of muscles – subepicardial fibers responsible for circumferential contraction and subendocardial longitudinal fibers.

Longitudinal fibers, when contracting, lead to approximation of the RV infundibulum to the tricuspid annulus, which is crucial for RV Ejection Fraction. Longitudinal contraction can be measured by TAPSE. The greater the descent of the base in systole, the better the RV systolic function.

In pulmonary embolism, TAPSE has been found to be an independent predictor of mortality and is now included in the PESI ECHO score.

Sensitivity and specificity, as well as evidence: Many studies have demonstrated the clinical utility of TAPSE. Although it measures longitudinal function, it has shown a good correlation with techniques that estimate RV global function. Diagnostic accuracy of TAPSE for reduced RV EF is Specificity 100%, Sensitivity 56%, Negative predictive value 56%, Positive predictive value 100% Barthélémy et al.

Alternative methods for obtaining similar information include subcostal echocardiographic assessment of the tricuspid annular kick (SEATAK) and the subcostal TAPSE (S-TAPSE).

Tricuspid Annular Peak Systolic Velocity (S’)

Tricuspid Annular Peak Systolic Velocity (TAPSV), also known as right ventricular S’, is a key echocardiographic measure of right ventricular systolic function. It reflects longitudinal myocardial contraction and is easily obtained using Tissue Doppler imaging.

S-wave measured as <10 cm/s on tissue Doppler imaging is associated with RV systolic dysfunction

Step-by-Step Guide for Tricuspid Annular Peak Systolic Velocity (S’) Measurement:

*Mode Required: Tissue Doppler

Tricuspid Annular Peak Systolic Velocity (S’) Interpretation

• S’ ≥ 10 cm/s → Normal RV systolic function.
• S’ < 10 cm/s → Suggests RV systolic dysfunction.
• Severely reduced S’ (< 7 cm/s) → May indicate significant RV failure.

POCUS 101 Extras:

A decreased S’ wave velocity on echocardiography (echo) can be suggestive of limited pulmonary vascular flow in patients with pulmonary embolism (PE). A low velocity S’ has  sensitivity of 90% and a specificity of 85%, yet  inferior to TAPSE for 30 day prediction of adverse outcomes in acute PE (J Meluzín. et al, Kurnicka et al.)

Right Ventricular Systolic Pressure (RVSP)

Estimating RVSP is a surrogate measurement for pulmonary artery systolic pressure which tells us the pressure generated by the right heart. Assuming that there is no RVOT obstruction, using Bernoulli equation, it can be estimated by measuring tricuspid regurgitation jet velocity to get the pressure gradiant between the Right atrium and the Right Ventricle and then adding the right atrial pressure to it to get the RVSP.

***In the absence of a gradient across the pulmonic valve or RVOT, PASP (pulmonary arterial systolic pressure) is equal to RVSP.

It is important to understand how the RVSP is calculated. It is basically the peak pressure gradient between the RV and the RA PLUS the Right Atrial Pressure (RAP)

Many beginners will equate the pressure gradient to the RVSP. Remember, you must also add the Right Atrial Pressure (RAP).

Step-by-Step Guide for RVSP Measurement:

*Mode Required: Continuous Wave Doppler

Step 5: Obtain an IVC view and estimate the RAP according to the table below.

IVC Size	IVC Collapsibility	Interpretation (CVP)
< 1.5cm	>50% collapsibility	0-5 mm Hg (Low CVP)
1.5-2.5cm	>50% collapsibility	6-10 mm Hg
1.5-2.5cm	<50% collapsibility	11-15 mm Hg
>2.5cm	<50% collapsibility	16-20 mm Hg (High CVP)

Step 6: Plug into the RVSP Equation:

RVSP = RV Pressure Gradient + RAP
RVSP = 4(V)² + RAP
*** Make sure to to use m/sec for the pressure gradient

For example if we use an example where patient has an RV Peak Pressure gradient of 3m/sec and assume we calculate an RAP of 10 mmHg based off IVC size and collapsibility. Then the RVSP would be the following:

RVSP = 4(3m/sec)² + 10 mmHg
RVSP = 4*9 mmHg + 10 mmHg
RVSP = 36 mmHg + 10 mmHg
RVSP = 46 mmHg

POCUS 101 Extras:

Increased estimated RVSP was associated with increased odds (OR – 1.35) of mortality in ICU patients with PE even after adjusted for APACHE score (Khemasuwan, et al). Another study reported pooled estimates of sensitivity and specificity of 47% and 73% respectively for transthoracic echocardiographic signs for diagnosis of PE (Fields, et al).

Right Ventricular Outflow Track (RVOT) VTI

The Right Ventricular Outflow Tract Velocity Time Integral (RVOT VTI) is a Doppler ultrasound measurement that represents the distance blood travels through the right ventricular outflow tract during one cardiac cycle. It is calculated by tracing the area under the Doppler velocity curve obtained from the RVOT, providing an estimate of the right ventricular stroke volume and overall cardiac output.

Step-by-Step Guide for RVOT VTI Measurement:

*Mode Required: Pulse Wave Doppler

RVOT VTI Interpretation:

Normal Range: 18–22 cm

<10 severe RV dysfunction (source?)

We will use RVOT VTI measurements to help calculate Pulmonary Vascular Resistance.

Pulmonary Artery Acceleration Time (PAAT)

The time from the start of RV ejection to the peak velocity is known as the Pulmonary Artery Acceleration Time (PAAT).This is also been referenced as Pulmonary Acceleration Time (PAT) or Pulmonary Valve Acceleration Time (PVAT). This can be measured as seen below and is the time (in milliseconds) from the start of flow to the peak of the RVOT VTI Waveform:

A normal PAAT is greater than 130msec. As pulmonary pressures increase and pulmonary hypertension worsens, the PAT will shorten.

• Normal: >130 ms
• Borderline: ~100–130 ms
• Mild Pulmonary Hypertension: ~60–100 ms
• Severe Pulmonary Hypertension: <60 ms

RVOT VTI Notching

As precapillary pulmonary hypertension progresses, the Doppler profile of the right ventricular outflow tract (RVOT) VTI undergoes characteristic changes that reflect rising pulmonary vascular resistance with the presence of “notching.” (Hockstein, Haycock, et al 2021)

Early Changes (Image A):
The waveform loses its smooth, rounded contour and begins to take on a sharper, “V-shaped” appearance. This transformation is accompanied by a reduction in pulmonary artery acceleration time (PAAT), also know as pulmonary valve acceleration time (PVAT) —the interval from the start of flow to peak velocity—shifting the peak velocity earlier in systole.

Mid-Stage Changes (Image B):
As pulmonary vascular resistance increases, a notch may appear in mid-systole, indicating disrupted forward flow due to wave reflection. This systolic notching is more typical of precapillary pathology and is often absent in purely postcapillary disease.

Advanced Disease (Image C):
In severe cases, the waveform becomes markedly abbreviated and takes on a spike-like shape, reflecting extremely rapid deceleration of flow and severely elevated pulmonary pressures.

Tracking these waveform changes—and particularly noting the presence of a systolic notch—can help clinicians distinguish precapillary from postcapillary pulmonary hypertension and gauge disease severity using noninvasive echocardiographic tools.

Pulmonary Vascular Resistance

Once the Max TR velocity and RVOT VTI are obtained, PVR is calculated using the following ratio: TRV/RVOT VTI. Where TRV is the Max Tricuspid Regurgitant Velocity in m/s. Then, depending on the TRV/RVOT VTI ratio and/or the presence of notching in the RVOT VTI, different formulas can be used to calculate the PVR (in Woods Units) using the algorithm below:

TRV = Max Tricuspid Regurgitant Velocity in m/s.
PASP = 4 x TRV² + 8mmHg. ***They did not measure IVC and just put RAP as 8mmHg for all patients.

• Lower PVR (<3 Wood units) is considered normal.
• Higher PVR (>3 Wood units) suggests pulmonary hypertension.

60/60 Sign

The 60/60 sign reflects two key hemodynamic changes indicative of an acute increase in right-sided pressure (Kurzyna, et al).

Tricuspid Regurgitation (TR) Pressure Gradient < 60 mmHg – This suggests RV dysfunction, as an acutely strained right ventricle lacks the ability to generate higher pressures.

*POCUS 101 Editor’s Note: the 60/60 sign using the TR Pressure gradient NOT the RVSP. So do NOT add the RAP to the gradient.

Pulmonary Artery Acceleration Time (PAAT) < 60 milliseconds – This is the interval from the onset of systolic blood flow in the pulmonary artery to its peak velocity. It serves as a marker of right ventricular afterload; higher resistance against the RV results in a shorter PAAT.

The combination of these two findings is valuable in assessing RV strain and differentiating acute RV failure (as seen in massive pulmonary embolism) from chronic RV failure (due to pulmonary hypertension). In chronic cases, the RV undergoes hypertrophy and can generate a TR pressure gradient > 60 mmHg.

60/60 sign has been generally reported to have poor sensitivity but good specificity in diagnosing PE or precisely acute elevation in pulmonary artery pressure. 

Overall, data on the sensitivity and specificity of 60/60 is limited, but studies have reported a sensitivity of 13 to 51% and a specificity of 69 to 96%.

Venous Congestion Evaluation – VExUS Score

Another extremely helpful quantitative measurement that can be done is to calculate the VExUS score. You can read the full post on VExUS HERE.

The VExUS score measures venous congestion and can help assess the downstream effects of significant right heart failure on the liver, gut, and kidneys.

In addition, the VExUS score can help assess if management of RV failure is improving venous congestion.

Specific Right Heart Diseases

Pulmonary Embolism

Pulmonary embolism (PE) is a life-threatening condition where timely diagnosis is critical, especially in unstable patients. Point-of-care ultrasound (POCUS) can rapidly identify signs of acute right heart strain that support the diagnosis and guide emergent care.

Ultrasound Features of PE:

• Right Ventricular Enlargement: An RV that appears equal to or larger than the LV on apical four-chamber, subxiphoid, or parasternal views is concerning for RV pressure overload. A ratio of RV to LV >1 is abnormal, and values >1.5 indicate severe dilation. Although not sensitive, this has high specificity for PE.
• Septal Flattening (“D Sign”): In the parasternal short-axis view, the LV may take on a D shape due to right-sided pressure pushing the septum leftward. This typically occurs in systole and diastole when pressure overload is present and suggests acute RV strain. The eccentricity index (EI), calculated as D2/D1, is >1 in these cases.
• McConnell’s Sign: This refers to a pattern where the RV apex is hyperdynamic while the mid-free wall shows reduced motion. This regional dysfunction is a marker of acute RV overload and has strong specificity for PE when present.
• 60/60 Pattern: A pulmonary acceleration time under 60 ms combined with a tricuspid regurgitant pressure gradient below 60 mmHg suggests sudden increases in RV afterload, often due to PE. Although this finding isn’t sensitive, its specificity is high.
• Reduced RV Longitudinal Function (TAPSE): TAPSE values under 16 mm reflect impaired systolic function of the right ventricle. Low TAPSE is associated with increased mortality in PE and is included in severity scoring tools.
• S’ Velocity: Tissue Doppler assessment of the tricuspid annulus may show an S’ wave under 10 cm/s, suggesting reduced contractility. While not PE-specific, it supports RV dysfunction.
• RVOT VTI and Systolic Notching: A shortened velocity time integral (VTI) of the RV outflow tract—especially under 10 cm—or the presence of a mid-systolic notch indicates elevated pulmonary vascular resistance and is consistent with PE-related strain.
• Visible Thrombus in the Right Heart: Identifying a mobile clot in the right atrium or ventricle is rare but highly specific. It signifies a clot en route to the lungs and carries high mortality risk.
• Dilated IVC with Low Collapsibility: A large, non-collapsing inferior vena cava implies high right atrial pressure. While not diagnostic, it complements other findings of RV strain.

Clinical Significance

When multiple signs of RV strain are observed—particularly RV enlargement, McConnell’s sign, and the D sign—in a patient with suggestive symptoms, PE should be strongly suspected. In critically ill patients where CT angiography is delayed or contraindicated, ultrasound provides valuable bedside information that can impact immediate management and risk stratification.

Here are the recommendations from the PERT Consortium:

Acute Respiratory Distress Syndrome (ARDS)

ARDS imposes significant stress on the right side of the heart due to elevated pulmonary pressures, hypoxic vasoconstriction, and the effects of mechanical ventilation. POCUS offers a real-time window into RV performance and helps detect early signs of strain, allowing for tailored interventions.

Ultrasound Features of ARDS:

• RV Enlargement (RV/LV Ratio): When the RV appears equal to or larger than the LV in apical or parasternal views, it suggests volume or pressure overload—common in ARDS due to increased pulmonary resistance and PEEP settings.
• Septal Flattening (D Sign): A D-shaped left ventricle in parasternal short axis view indicates RV overload. If present during both systole and diastole, this points to significant pressure elevation, often seen in advanced ARDS.
• TAPSE and S’ Abnormalities: TAPSE <16 mm or S’ velocity <10 cm/s signifies reduced RV longitudinal function. These findings reflect impaired systolic performance, which can worsen with ongoing ventilator-induced pressure load.
• Elevated RVSP: A high RV systolic pressure, derived from tricuspid regurgitation velocity plus estimated right atrial pressure, suggests increased pulmonary afterload. This can drive RV dysfunction and right heart failure if left unaddressed.
• Abnormal RVOT Doppler: A short pulmonary acceleration time (PAT <130 ms), especially if under 60 ms, and the presence of mid-systolic notching on RVOT VTI waveform suggest precapillary pulmonary hypertension—often reversible in ARDS with appropriate therapy.

• When PVR is Elevated: A calculated PVR >3 Wood units suggests elevated resistance within the pulmonary vasculature. In cases of high PVR, targeted pulmonary vasodilators or inodilators (e.g., milrinone, inhaled nitric oxide, or prostacyclin) may be beneficial. These reduce afterload on the RV, improving forward flow and cardiac output.
• When PVR is Normal or Low: If PVR is not significantly elevated, use of vasodilators can be harmful, as they may cause systemic hypotension without improving RV output. In such cases, management should focus instead on ventilator optimization and volume status.

By tailoring treatment based on PVR assessment, clinicians can avoid inappropriate therapies and direct support where it’s most effective—either reducing RV afterload or focusing on preload and ventilator adjustments.

Why This Matters

ARDS creates a high afterload state for the right ventricle, especially in patients requiring mechanical ventilation. Recognizing early signs of RV dysfunction with ultrasound allows for timely adjustments in ventilator settings (e.g., reducing PEEP), fluid strategies, or consideration of pulmonary vasodilators. Frequent POCUS assessments can track response to interventions and guide management to prevent right heart failure.

Right Sided Myocardial Infarction

Right-sided myocardial infarction can result in acute RV failure, hemodynamic instability, and significant preload sensitivity. Prompt identification with POCUS can help guide fluid resuscitation, inotropic support, and avoid interventions that may worsen the clinical picture.

Ultrasound Features in RVMI

• RV Enlargement: The right ventricle may appear dilated compared to the left ventricle in apical four-chamber or subxiphoid views. This enlargement is often acute and associated with hypotension and clear lungs, especially in isolated RV infarction.
• Wall Motion Abnormalities: In RVMI, the RV free wall often shows diffuse hypokinesis, including the apex. This contrasts with McConnell’s sign seen in PE, where the apex is typically hyperdynamic. Global or inferior wall dysfunction suggests ischemia rather than pressure overload.
• Decreased TAPSE and S’ Wave: TAPSE less than 16 mm and S’ velocity below 10 cm/s reflect impaired RV contractility. These findings support the diagnosis of RV infarction when present alongside clinical signs.
• Dilated IVC with Poor Collapse: A plethoric IVC that shows minimal respiratory variation indicates elevated right atrial pressure and supports the need for cautious volume loading to optimize preload.
• Normal or Mildly Elevated RVSP: Since RVMI is not primarily a pressure overload issue, estimated RV systolic pressures often remain within normal range unless complicated by left-sided dysfunction or pulmonary pathology.

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Summary

Bedside ultrasound is an invaluable tool for identifying right-sided myocardial infarction. Key features include global RV dysfunction (including apex), a dilated and hypokinetic right ventricle, reduced longitudinal function, and a distended IVC. These findings distinguish RVMI from pulmonary embolism and guide clinicians to prioritize preload optimization and inotropic support while avoiding vasodilators or diuretics.

Post-Capillary Pulmonary Hypertension (Left Sided Heart Failure)

Heart failure with preserved ejection fraction (HFpEF)

Heart failure with preserved ejection fraction (HFpEF) can lead to elevated left-sided filling pressures, which in turn increase pulmonary venous pressure and result in post-capillary pulmonary hypertension. Unlike precapillary causes, this form of RV strain stems from backward transmission of pressure rather than elevated pulmonary vascular resistance. Ultrasound helps clarify the hemodynamics and detect subtle signs of right heart involvement.

Ultrasound Features in HFpEF-Related Pulmonary Hypertension

• Normal or Mild RV Dilation: RV size may be preserved or only mildly enlarged, especially early in the disease process. When RV enlargement is present, it often develops slowly due to chronic pressure elevation.
• Intermittent D Sign: In post-capillary pulmonary hypertension, septal flattening may occur but is often more pronounced during diastole rather than systole. This pattern reflects volume overload as opposed to pressure overload seen in precapillary disease.
• Preserved or Mildly Reduced TAPSE and S’: RV longitudinal function may remain intact until late stages. TAPSE >16 mm and S’ velocity >10 cm/s are common early on, but progressive decline may occur with worsening pulmonary pressures and RV remodeling.
• Elevated RVSP: This is often the most prominent finding. Tricuspid regurgitation velocity is typically increased, and when combined with elevated right atrial pressure (based on IVC size and collapsibility), estimated RVSP reflects elevated left atrial and pulmonary venous pressures.
• No RVOT Notching: Unlike precapillary pulmonary hypertension, the RVOT Doppler waveform is typically smooth, and pulmonary acceleration time is not significantly shortened. The absence of mid-systolic notching helps differentiate post-capillary from precapillary etiologies.
• Dilated IVC with Decreased Collapse: The IVC may appear distended with reduced respiratory variation, indicating elevated right-sided filling pressures. In HFpEF, this reflects chronically transmitted pressure from the left heart.

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Summary

In HFpEF-related post-capillary pulmonary hypertension, ultrasound reveals elevated RVSP, often with a preserved RV size and function early in the disease course. The absence of RVOT notching and the presence of a dilated IVC further support a passive, volume-driven cause of RV strain. Recognizing this pattern helps clinicians differentiate post- from precapillary disease and avoid unnecessary vasodilators, focusing instead on volume management and left-sided unloading strategies.

Heart failure with reduced ejection fraction (HFrEF)

In heart failure with reduced ejection fraction (HFrEF), chronic elevation of left-sided pressures can lead to pulmonary venous congestion and ultimately post-capillary pulmonary hypertension. Over time, this increases the workload on the right ventricle, potentially resulting in RV dilation, dysfunction, and secondary tricuspid regurgitation. POCUS is essential for evaluating the downstream impact of left ventricular failure on the right heart and guiding appropriate therapy.

Ultrasound Findings in HFrEF with RV Involvement

• Dilated RV: In contrast to HFpEF, HFrEF more often leads to significant RV remodeling over time. An enlarged RV in the apical four-chamber view (RV/LV ratio >1.0) may indicate advanced disease and chronic pulmonary venous hypertension.
• Reduced RV Function: Longitudinal dysfunction is frequently seen. TAPSE <16 mm and S’ <10 cm/s are common and may progress with worsening biventricular failure.
• Elevated RVSP: Tricuspid regurgitation velocity is typically high due to increased pulmonary venous pressures transmitted backward. Estimating RVSP using TR velocity plus IVC-derived RAP gives insight into pulmonary artery pressures, which are often elevated in chronic HFrEF.
• D Sign with Mixed Patterns: Septal flattening may be present but tends to reflect volume overload more than pressure overload, and may vary with the stage of heart failure and fluid status.
• Dilated IVC with Poor Collapsibility: A full, non-collapsing IVC suggests elevated right atrial pressure and systemic congestion—key signs of right-sided decompensation in HFrEF.
• Normal RVOT Contour (No Notch): The Doppler waveform through the RV outflow tract generally lacks the mid-systolic notching typical of precapillary disease. Pulmonary acceleration time may be mildly reduced, but the overall pattern remains smooth.

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Summary

In HFrEF-related post-capillary pulmonary hypertension, ultrasound often reveals biventricular dysfunction: a dilated and weakened RV, elevated RVSP, and signs of systemic congestion such as a dilated IVC. The absence of RVOT notching helps differentiate this chronic volume-driven strain from acute or precapillary causes. Recognizing this profile supports strategies that prioritize afterload reduction, diuresis, and optimization of LV function.

Pre-Capillary Pulmonary Hypertension

Pre-capillary pulmonary hypertension refers to elevated pulmonary artery pressures originating from pathology within the pulmonary vasculature itself—such as pulmonary arterial hypertension (PAH), chronic thromboembolic disease, or hypoxic pulmonary vasoconstriction—not from left heart disease. Over time, this increased afterload leads to progressive right ventricular strain and dysfunction. POCUS enables early recognition of these changes and helps differentiate pre-capillary from post-capillary causes.

Ultrasound Features of Pre-Capillary PH

• Right Ventricular Dilation: A markedly enlarged RV compared to the LV (RV/LV ratio >1.0 or even >1.5) is a hallmark finding. This is often most apparent in apical four-chamber or subxiphoid views.
• D Sign (Septal Flattening): A classic indicator of RV pressure overload. In pre-capillary PH, the interventricular septum shifts leftward during both systole and diastole, producing a D-shaped LV in parasternal short-axis view. This indicates chronically elevated right-sided pressures.
• RV Dysfunction (TAPSE & S’): As RV pressure load increases, systolic function declines. TAPSE <16 mm and S’ <10 cm/s on tissue Doppler suggest impaired longitudinal contraction and are common in moderate to severe disease.
• RVOT VTI Notching and Shortened Acceleration Time: In pre-capillary PH, the RVOT Doppler waveform shows a shortened pulmonary acceleration time (PAT <100 ms, often <60 ms in severe cases). Mid-systolic notching is a classic finding and is typically absent in post-capillary PH.
• IVC Distension with Minimal Collapsibility: A dilated IVC with <50% collapse supports elevated right atrial pressure and systemic venous congestion, which develops in later stages.

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