{"id":2606,"date":"2026-04-26T18:00:00","date_gmt":"2026-04-26T18:00:00","guid":{"rendered":"https:\/\/emultrasound.ucsd.edu\/?p=2606"},"modified":"2026-04-25T17:50:56","modified_gmt":"2026-04-25T17:50:56","slug":"case-67-d-sign-in-a-post-cardiac-surgical-patient","status":"publish","type":"post","link":"https:\/\/emultrasound.ucsd.edu\/index.php\/2026\/04\/26\/case-67-d-sign-in-a-post-cardiac-surgical-patient\/","title":{"rendered":"Case 67: D-sign in a Post-Cardiac Surgical Patient"},"content":{"rendered":"\n

Liz Temple, Colleen Campbell<\/p>\n\n\n\n

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

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

Vitals:<\/strong> BP 128\/75 | Pulse 86 | Temp 97.7 \u00b0F (36.5 \u00b0C) | Resp 17 | SpO2 98% | BMI 24.4 kg\/m\u00b2<\/p>\n\n\n\n

Physical Exam:<\/strong><\/p>\n\n\n\n

Gen: well appearing, NAD<\/p>\n\n\n\n

HEENT: normocephalic, atraumatic, moist mucous membranes, sclera anicteric, EOMI<\/p>\n\n\n\n

CV: WWP, RRR, radial pulses 2+, JVP ~9cm<\/p>\n\n\n\n

Resp: no increased work of breathing, no accessory muscle use, speaks in full<\/p>\n\n\n\n

sentences, breathing comfortably on RA, CTAB<\/p>\n\n\n\n

Abd: soft, nontender, nondistended<\/p>\n\n\n\n

Ext: no lower extremity edema<\/p>\n\n\n\n

Neuro: moves all limbs spontaneously, no facial asymmetry, no dysarthria, EOMI<\/p>\n\n\n\n

Labs<\/strong>: Troponin within normal limits<\/p>\n\n\n

\n
\"\"
Figure 1.<\/strong>\u00a0Cardiac POCUS with parasternal long axis showing dilated right ventricle (RV). No evidence of a significant pericardial effusion although there appears to be an echogenic focus on anterior RV free wall.<\/figcaption><\/figure>\n<\/div>\n\n\n
\"\"
Figure 2: Parasternal short axis view from formal echocardiogram displaying the \u201cD-sign\u201d of right ventricular strain. <\/figcaption><\/figure>\n\n\n\n
\"\"
Figure 3: Apical 4-chamber view from formal echocardiogram demonstrating septal bowing into left ventricle most prominently during diastole. <\/figcaption><\/figure>\n\n\n\n

Discussion<\/strong><\/p>\n\n\n\n

The \u201cD-sign\u201d on cardiac POCUS can help to identify right heart strain of varying etiologies, and is often considered a canonical sign for pulmonary embolism. This finding is most clearly visualized using a parasternal short axis view where the left ventricle appears as a D-shaped structure as a result of right ventricular overload which causes the interventricular septum to bow towards the left heart.1,2<\/sup><\/p>\n\n\n\n

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

More specifically, right ventricular strain can be stratified by whether it is a result of pressure overload versus volume overload. In a patient with right ventricular pressure overload, elevated pressures on the right side are present both during systole and diastole, and therefore the left ventricular \u201cD-shape\u201d is present throughout the cardiac cycle. Pathologies that correlate with right ventricular pressure overload include pulmonary embolism, pulmonary hypertension, chronic right hear failure with hypertrophy, left-sided heart failure, and ARDS. Conversely, in patients with right ventricular volume overload, the sequelae of volume overload are most apparent during diastolic filling, so the D-sign is most obvious at end diastole while the left ventricle appears more normal and circular shaped during end-systole.4<\/sup> Conditions that correlate with right ventricular volume overload may include severe tricuspid regurgitation, decompensated heart failure, and excessive volume resuscitation.1<\/sup><\/p>\n\n\n\n

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

\n
\"\"
Figure 4: Eccentricity index calculation to distinguish between right ventricular pressure and volume overload. Source: Pocus 101<\/a><\/figcaption><\/figure>\n<\/div>\n\n\n

In this particular case, it is clear that the interventricular septal bowing is variable throughout the cardiac cycle (Figure 1-3) and the D-sign is most evident at end diastole which would suggest a \u2018volume overload\u2019 subset of RV strain. Moreover, the EI follows a pattern consistent with right ventricular volume overload, although this was not measured during the formal echo. The etiology of this volume overload RV strain may have been partly attributed by volume overload as he had an elevated JVD and a plump IVC on formal echo. However, considering the context of his recent open-heart surgery with pericarditis and evidence of RV free wall mobility limitation (Figure 3), there was higher suspicion for external compression or inflammation as the cause of his rapid onset RV dysfunction. A subsequent CT scan suggested evidence of possible pericardial clot resulting in external RV compression. The patient was subsequently scheduled for left and right heart catheterization for further assessment of cardiac pressures as a result of this new onset RV strain on ultrasound before proceeding with further surgical intervention.<\/p>\n\n\n\n

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

References:<\/strong><\/p>\n\n\n\n

    \n
  1. Dinh V. The D Sign - Right Heart Strain from Pressure vs Volume Overload. POCUS 101<\/em>, https:\/\/www.pocus101.com\/the-d-sign-right-heart-strain-from-pressure-vs-volume-overload\/ (accessed October 17, 2025).<\/li>\n\n\n\n
  2. Cativo Calderon EH, Mene-Afejuku TO, Valvani R, et al. D-shaped left ventricle, anatomic, and physiologic implications. Case Rep Cardiol<\/em> 2017; 2017: 4309165.<\/li>\n\n\n\n
  3. Fields JM, Davis J, Girson L, et al. Transthoracic echocardiography for diagnosing pulmonary embolism: A systematic review and meta-analysis. J Am Soc Echocardiogr<\/em> 2017; 30: 714-723.e4.<\/li>\n\n\n\n
  4. Tanaka H, Tei C, Nakao S, et al. Diastolic bulging of the interventricular septum toward the left ventricle. An echocardiographic manifestation of negative interventricular pressure gradient between left and right ventricles during diastole. Circulation<\/em> 1980; 62: 558\u2013563.<\/li>\n\n\n\n
  5. Ryan T, Petrovic O, Dillon JC, et al. An echocardiographic index for separation of right ventricular volume and pressure overload. J Am Coll Cardiol<\/em> 1985; 5: 918\u2013927.<\/li>\n<\/ol>\n\n\n\n

    <\/p>\n","protected":false},"excerpt":{"rendered":"Liz Temple, Colleen Campbell A 51-year-old male patient with past medical history of mitral valve prolapse s\/p complex mitral valve repair with left atrial appendage exclusion and repair of atrial septal defect complicated by perioperative pericarditis was directly admitted to the ICU following outpatient echocardiography findings of new right heart strain. Since his open heart …

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