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Echocardiographic Signs of Right Ventricular Strain in Acute Pulmonary Embolism

Updated: Apr 9

Right ventricular (RV) strain, as seen on echocardiography, is a common finding in patients with pulmonary embolism (PE). This is due to the increased workload on the right side of the heart in order to compensate for the blockage in the pulmonary arteries. It is crucial for intensivists to recognize these echocardiographic findings and understand their pathophysiology, as they could suggest a diagnosis of submassive or massive PE. Timely management in PE is crucial as it is a potentially life-threatening condition. RV strain, when observed in conjunction with other clinical findings, can aid in making a timely diagnosis and initiation of treatment. These signs include basal RV/LV ratio >0.9, D sign, McConnell's sign, TAPSE, 60/60 sign, RV velocity (S'). The intensivist can also easily obtain the first four signs with the bedside ultrasound with some training, while the last 2 signs (60/60 and S') require continuous wave (CW) doppler and pulse wave tissue doppler imaging (TDI). Other important signs such as the pulmonary artery mid-systolic notching, and the speckle tracking are not going to be discussed here.

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Basal RV/LV > 0.9

In the RV-focused apical 4 chamber view, a right ventricle basal diameter of >4.2 cm, a mid-cavity diameter of >3.5 cm, and a length greater than 8.6 cm indicate RV dilation. A ratio of the right and left ventricular end-diastolic basal diameters greater than 0.9 strongly suggests RV strain.

The RV:LV >0.9 had a sensitivity of 91.7 percent and a specificity of 75 percent, according to one research [1]. CT scan may be used to evaluate the RV/LV ratio and strain in the right ventricle as well.

The D-sign

The D sign is indicative of right ventricular overload. This means there is too much pressure or volume being placed on the right ventricle, causing it to push the septum towards the left side and giving the right ventricle a D shape. Although the sign is associated with RV strain in pulmonary embolism, it can also be found in other forms of pressure overload, such as pulmonary hypertension, left-sided heart failure, and ARDS, or volume overload conditions including severe tricuspid regurgitation, aggressive volume resuscitation, or decompensated heart failure. It is important to mention that D sign is seen in both diastole and systole in pressure overload, while it is only seen in diastole in volume overload.

McConnell's sign

McConnell's sign is named after British radiologist J. McConnell and is determined by observing the motion of the right ventricle's apex during systole. In cases of pulmonary embolism, there is a normal wall motion at the apex and abnormal wall motion in the mid-free wall of the right ventricle. McConnell's sign has been found to have variable sensitivity and specificity for diagnosing pulmonary embolism. McConnell et al. in their original study showed that this sign had a 77 percent sensitivity and a 94 percent specificity for the detection of acute pulmonary embolism, with a positive predictive value of 71% and a negative predictive value of 96% [2]. However, subsequent studies have shown that it can be seen in acute RV infarct and in patients with chronic pulmonary hypertension. Casazza et al. found that the McConnell sign was only 70% sensitive and 33% specific for diagnosing pulmonary embolism. Its positive predictive value was 67%, and its negative predictive value was 36% [3]. Though It is valuable, it should not be viewed as the only evidence of pulmonary embolism. Instead, it should be used in conjunction with other medical evaluations and imaging echocardiographic signs for an accurate diagnosis of pulmonary embolism.

Tricuspid Annular Plane Systolic Excursion (TAPSE) <16 mm

Tricuspid annular plane systolic excursion (TAPSE) is a measure of the motion of the tricuspid valve and can be used as a marker for right ventricular function. TAPSE can be assessed in the M-mode by placing the cursor at the level of the lateral aspect of the tricuspid annulus and measuring the maximum displacement with systole. TAPSE values less than 16 mm were considered abnormal (a TAPSE of less than 18 mm was considered abnormal in other references.). ROC curve analysis was used to determine the optimal TAPSE measurement for identifying clinically significant aPE in one study. The sensitivity of 53.33% (95% CI 26.67%–80.00%) and the specificity of 100% (95%, CI 100–100) were measured when the cutoff TAPSE measurement was 15.2 mm [4].

60/60 Sign

The 60/60 sign, which combines a right ventricular systolic pressure (RVSP) less than 60 mmHg and a pulmonary valve acceleration time (PAT) less than 60 milliseconds, has been evaluated as a marker of acute right ventricular strain. The sensitivity and specificity of the test were 70.83 percent and 93.75 percent, respectively, according to one research [1].

The RVSP is calculated by taking the tricuspid regurgitation jet gradient obtained by continuous wave doppler, plus the projected right atrial pressure from the IVC diameter. Because chronic pulmonary hypertension is required for a very high RVSP to be generated, it's logical that an RVSP of 60 mmHg or less implies an acute condition.

The pulmonic valve acceleration time is the amount of time it takes for the pulmonic velocity to reach a peak and is obtained by pulse wave doppler. A distal, persistent pulmonary arterial hypertension would result in a longer PAT as the summative compliance of the pulmonary vessels accepts RV output more slowly before it peaks (similar to blowing up a huge balloon). In contrast, an obstructive lesion at the proximal level causes the velocity to peak quickly V inflation with low little vascular compliance (similar to blowing through an obstructed straw).

Decreased RV Velocity (S')

The RV velocity (s') is measured by pulsed wave Tissue Doppler imaging in the apical four-chamber view at the junction of the RV free wall and tricuspid annular plane. S' wave velocity is a measure of the speed of the tricuspid annulus during systole, and it is above 10 cm/s in a normal RV function. It represents the maximum velocity achieved by the lateral tricuspid annulus during systole, and it has more significance than TAPSE since it is not subject to angle variation. In patients with pulmonary embolism, a decreased S' wave velocity suggests restricted pulmonary vascular flow [5].


There are several echocardiographic signs that aid the intensivist in determining whether a right ventricular strain is present in acute pulmonary embolism. However, all of these signs should be interpreted in the context of the patient's clinical presentation and other diagnostic tests. It is important to note that echocardiography alone cannot confirm a diagnosis of pulmonary embolism, but it can aid in determining appropriate management decisions.


  1. Shah BR, Velamakanni SM, Patel A, Khadkikar G, Patel TM, Shah SC. Analysis of the 60/60 Sign and Other Right Ventricular Parameters by 2D Transthoracic Echocardiography as Adjuncts to Diagnosis of Acute Pulmonary Embolism. Cureus. 2021 Mar 10;13(3):e13800. doi: 10.7759/cureus.13800. PMID: 33842172; PMCID: PMC8033646.

  2. McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. The American journal of cardiology. 78(4):469-73. 1996.

  3. Casazza F, Bongarzoni A, Capozi A, Agostoni O. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction. Eur J Echocardiogr. 2005;6(1):11-4.

  4. Lahham S, Fox JC, Thompson M, Nakornchai T, Alruwaili B, Doman G, May Lee S, Shafi A, Shniter I, Valdes V, Zhang L. Tricuspid annular plane of systolic excursion to prognosticate acute pulmonary symptomatic embolism (TAPSEPAPSE study). J Ultrasound Med. 2019 Mar;38(3):695-702. doi: 10.1002/jum.14753. Epub 2018 Sep 4. PMID: 30182486; PMCID: PMC6628892.

  5. Kjaergard J, Schaadt BK, Lund JO, Hassager C. Quantification of right ventricular function in acute pulmonary embolism: relation to extent of pulmonary perfusion defects. Eur J Echocardiogr. 2008;9:641–645

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