Echocardiography (TTE)

Clinical Case Study and Scenario Exploration

A Case of D-Shaped Left Ventricle: Recognizing Acute Right Ventricular Failure (Written December 13, 2024)

Abstract

A middle-aged female patient presented with a two-week history of progressive dyspnea and fluid retention. Imaging studies, including chest radiography and computed tomography (CT), revealed severe pulmonary edema, pleural effusion, and ascites. Transthoracic echocardiography identified a D-shaped left ventricle, suggesting acute right ventricular (RV) pressure overload. Despite the absence of a clear underlying cause, such as pulmonary embolism, her hemodynamic status deteriorated rapidly. This case emphasizes the importance of promptly recognizing acute right heart failure and the need for urgent referral when no immediate etiologic factor is identified.

Introduction

Acute right heart failure can be life-threatening, often progressing rapidly and posing management challenges distinct from chronic right-sided dysfunction. While left-sided heart failure is more common and well-characterized, acute right-sided failure demands prompt identification and intervention due to its potential for rapid clinical decline. Echocardiographic evidence of a D-shaped left ventricle strongly suggests RV pressure overload and can serve as an immediate clue to underlying acute right heart stress. This report details a case in which a patient with acute right ventricular failure and a D-shaped left ventricle was urgently referred for advanced care, highlighting the importance of timely diagnosis and management.

Case Presentation

A female patient in her fifth decade of life presented with a two-week history of progressively worsening dyspnea and edema. Prior to admission, she had been receiving care at a non-specialized medical facility, delaying advanced cardiopulmonary assessment. On evaluation, she exhibited severe respiratory distress and systemic congestion. A chest radiograph demonstrated marked pulmonary edema. Additional CT imaging revealed significant pleural effusions and ascites, yet no evidence of pulmonary embolism or other structural cardiopulmonary abnormalities was noted.

Transthoracic echocardiography revealed a characteristic D-shaped deformation of the left ventricle, reflecting interventricular septal shifting due to elevated RV pressure or volume load. Only mild tricuspid regurgitation (grade I) was observed, which does not align with the profound regurgitation typically seen in chronic right-sided failure, thus suggesting an acute process. Despite extensive evaluation, the immediate precipitant of acute RV strain could not be identified.

Given the patient’s severe condition and the rapid progression of symptoms, initial management focused on stabilizing intravascular volume with intravenous diuretics. With the imminent risk of hemodynamic collapse, the patient was urgently transferred to a tertiary care university hospital for further advanced diagnostic evaluation and potential intervention.

Key Concepts

• Right Ventricular (RV) Failure: A critical condition where the right ventricle fails to adequately pump blood into the pulmonary circulation.
• D-Shaped Left Ventricle (LV): An echocardiographic sign suggestive of RV pressure overload, altering the normal round shape of the LV into a D-shape due to septal displacement.

Background

Why is Right Ventricular Failure Unique?

• The RV is thinner-walled and more compliant than the LV, making it more sensitive to sudden increases in afterload (e.g., acute pulmonary hypertension).
• Acute RV failure can develop rapidly and may cause severe hemodynamic instability before obvious clinical signs arise.
• Unlike LV failure, which often presents with more recognizable patterns and established etiologies (e.g., ischemic heart disease, hypertensive heart disease), RV failure can be triggered by less common and more elusive conditions, making early recognition challenging.

Pathophysiological Mechanisms Leading to RV Failure:

1. Increased Afterload: Sudden rises in pulmonary arterial pressure (e.g., acute pulmonary embolism, severe acute pulmonary hypertension).
2. Direct Myocardial Injury: Isolated RV infarction, myocarditis predominantly affecting the right heart.
3. Volume Overload: Rapid fluid shifts or conditions causing abrupt RV dilation.
4. External Constraints: Pericardial tamponade or constrictive processes can indirectly compromise RV filling.

Common Etiologies of Acute RV Failure

Note: In this case, PE was ruled out early via CT.

Case Presentation (Re-Visited)

Patient Profile:

• A middle-aged female
• Chief complaint: Progressive dyspnea and edema for 2 weeks

Initial Findings:

• Severe Respiratory Distress: Marked shortness of breath, orthopnea
• Imaging:
  • Chest X-ray: Severe pulmonary edema (whited-out lung fields)
  • CT: Significant pleural effusions, ascites, but no pulmonary embolism or mechanical obstruction

Echocardiography Key Finding:

• D-Shaped LV: The interventricular septum bowing into the LV, strongly indicating increased RV pressure/strain
• Minimal Tricuspid Regurgitation: Suggesting this is an acute event, not a long-standing chronic RV failure

Suspected Mechanisms in this Case:

• Acute Pulmonary Hypertension of Unclear Origin: Possibly autoimmune (e.g., Takayasu arteritis) or a rapidly evolving inflammatory process.
• Non-Embolic RV Strain: Given that PE was excluded, other causes of acute RV stress must be considered.

Interpreting the D-Shaped LV

Why the LV Becomes D-Shaped:

• Under normal conditions, the LV cavity is elliptical.
• Increased RV pressure (due to high afterload or volume) pushes the interventricular septum into the LV cavity.
• On the parasternal short-axis view of an echocardiogram, this creates a "D-shaped" appearance rather than the normal circular LV contour.

Implications of a D-Shaped LV:

• Strongly suggests RV pressure overload.
• Often associated with conditions like acute PE, severe pulmonary hypertension, or acute RV decompensation.
• In chronic RV failure, one would expect more pronounced tricuspid regurgitation and RV dilation. The absence of these findings here points towards an acute process.

Differential Considerations in This Case

1. Acute Pulmonary Hypertension (e.g., autoimmune flare):
   • Possibly Takayasu arteritis or another vasculitis causing sudden rise in PA pressures.
   • Systemic autoimmune conditions can suddenly worsen, triggering acute pulmonary vascular changes.
2. Myocardial Process (e.g., Isolated RV Myocarditis):
   • Less common, but possible if inflammatory insults selectively target the RV.
3. Rare Embolic Sources (Non-Thrombotic):
   • Fat or air embolism, though these often have other clinical clues.

Diagnostic and Management Strategies

Initial Diagnostic Approach:

1. Exclude Common Causes First:
   • Pulmonary embolism ruled out by early CT scan.
   • No pericardial effusion or valvular lesion to suggest tamponade or severe valvular dysfunction.
2. Assess Hemodynamics:
   • RVSP ~54 mmHg: Elevated, but not as high as in longstanding severe RV failure, supporting an acute event.
3. Consider Specialized Tests:
   • Autoimmune markers, inflammatory tests.
   • Cardiac MRI or advanced imaging if stable enough.

Initial Management Measures:

• Volume Management:
  • Careful diuresis (e.g., intravenous loop diuretics) to relieve congestion.
  • Avoid aggressive fluid challenges in acute RV failure when pulmonary edema is present.
• Urgent Referral to Tertiary Center:
  • Potential access to advanced hemodynamic support (e.g., ECMO) if the patient deteriorates.
  • A multidisciplinary team (cardiology, pulmonary, rheumatology) to rapidly identify and manage any underlying cause.

Lessons Learned

• Rapid Decompensation Risk:
  • RV failure can worsen quickly. Early recognition is vital.
• D-Shaped LV as a Red Flag:
  • The "D-shape" on echo is a key visual sign indicating RV pressure overload.
• Diagnostic Complexity:
  • Unlike LV failure, which has more common etiologies, acute RV failure often arises from elusive or less typical conditions (e.g., autoimmune flares).
• Timely Transfer to Higher-Level Care:
  • When the diagnosis is unclear but the patient is unstable, prompt escalation of care is crucial.

Conclusion

Acute right ventricular failure presenting with a D-shaped left ventricle on echocardiography can present without classic etiologies like pulmonary embolism. In such scenarios, less common causes such as autoimmune-mediated acute pulmonary hypertension must be considered. Rapid recognition, careful volume management, and urgent referral to a tertiary care center for advanced diagnostic and therapeutic modalities are essential to improve patient outcomes.

Written on December 13th, 2024

D-Shaped Left Ventricle in Acute Pulmonary Embolism (Written December 13, 2024)

This work represents a rewritten interpretation of the original case study by Dr. Gabe Alagna (PGY1) and Dr. Lauren McCafferty, MD, intended to enhance understanding and facilitate learning for others while giving full credit to the original authors. A D-shaped left ventricle (LV) is a significant echocardiographic finding frequently observed when right ventricular (RV) pressures escalate. One critical clinical scenario associated with this pattern is acute pulmonary embolism (PE). For those seeking to broaden their understanding of the D-shaped LV in various clinical scenarios, a related case study is available at Intern Ultrasound of the Month: A Sign of Acute Pulmonary Embolism. This case, originally presented by Dr. Gabe Alagna (PGY1) and edited by Dr. Lauren McCafferty, MD (Alagna & McCafferty, 2024), features a 77-year-old female with a history of end-stage renal disease, heart failure, and lung cancer who presented to the emergency department after experiencing sudden unresponsiveness.

During her resuscitation for pulseless electrical activity (PEA) arrest, a cardiac point-of-care ultrasound was performed, revealing distinct echocardiographic findings indicative of acute PE, including marked RV enlargement and free wall hypokinesis with preserved apical contractility (McConnell’s sign). These findings, in conjunction with her underlying malignancy and abrupt hemodynamic deterioration, heightened the suspicion for an acute PE as the underlying cause of her clinical instability.

By reviewing this additional case, readers can gain a more comprehensive perspective on the various presentations and underlying mechanisms of a D-shaped LV. Comparing different etiologies, such as acute pulmonary embolism versus other causes of acute right ventricular failure, enhances the overall understanding of how this echocardiographic sign can manifest in diverse clinical contexts. Exploring multiple cases will aid in recognizing the nuanced differences and similarities, ultimately contributing to more accurate and timely diagnoses in emergency medicine.

This integrative approach underscores the importance of recognizing specific echocardiographic patterns, like the D-shaped LV and McConnell’s sign, within the broader clinical framework. Such recognition facilitates prompt and appropriate therapeutic interventions, thereby improving patient outcomes in acute and often life-threatening situations.

Case Overview

A 77-year-old female with a complex history, including end-stage renal disease, heart failure, and lung cancer, experienced a sudden change in mental status. She became unresponsive while seated, prompting activation of emergency medical services (EMS). Although initially awake during transport, she deteriorated upon arrival at the emergency department (ED) and suffered a pulseless electrical activity (PEA) cardiac arrest. Advanced Cardiac Life Support (ACLS) protocols were initiated. During a brief return of spontaneous circulation (ROSC), a point-of-care ultrasound (POCUS) examination revealed marked RV enlargement and free wall hypokinesis with relatively preserved apical contractility (McConnell’s sign). These findings raised strong suspicion for an acute PE, especially given the patient’s underlying malignancy and abrupt hemodynamic deterioration.

Key Echocardiographic Findings

• McConnell’s Sign:
  Characterized by akinesia or severe hypokinesis of the RV free wall with preserved apical contractility. Although not highly sensitive, it is highly specific for acute PE in the proper clinical context. McConnell’s sign may occasionally appear in RV ischemia unrelated to PE, but such occurrences are rare.
• RV Enlargement and D-Shaped LV:
  The RV-to-LV chamber size ratio often approaches or exceeds 1:1 in significant RV strain. Bowing of the interventricular septum into the LV yields a “D-shaped” appearance on short-axis echocardiographic views, reflecting RV pressure overload.
• Other RV Strain Indices:
  Additional parameters such as tricuspid annular plane systolic excursion (TAPSE) and abnormal septal motion (the “D sign”) support the diagnosis of acute PE when integrated with the entire clinical picture.

Diagnostic Considerations

Table: Key Differences in Echocardiographic Findings Between Acute PE-Related RV Strain and Other Causes

This table illustrates that while several findings may overlap between PE and other etiologies of RV dysfunction, the combination of McConnell’s sign and a D-shaped LV strongly directs attention to acute PE, particularly in the setting of hemodynamic instability and risk factors such as cancer-associated hypercoagulability.

Clinical Impact and Management Strategies

Acute PE spans a broad spectrum of severity, ranging from incidental findings in asymptomatic patients to sudden cardiovascular collapse. Hemodynamically unstable PE, once known as “massive” PE, demands rapid intervention. In this case, the recognition of McConnell’s sign prompted immediate therapeutic decisions. Systemic thrombolysis (IV tPA) was administered during recurrent PEA arrest, leading to ROSC. Subsequent stabilization permitted confirmatory imaging via CT angiography, which demonstrated a saddle PE.

1. Immediate Stabilization:
   Ensure airway patency, adequate oxygenation, and hemodynamic support. Vasopressors, fluids, and, in select cases, mechanical circulatory support can be employed.
2. Echocardiographic Assessment:
   Rapid bedside ultrasound can detect RV dilatation, reduced RV contractility, McConnell’s sign, and septal flattening. These findings guide further diagnostic and therapeutic steps, especially when hemodynamic instability precludes safe transfer for CT imaging.
3. Therapeutic Decision-Making:
   Initiation of anticoagulation is fundamental. In severe cases (e.g., persistent hypotension, recurrent arrest), systemic thrombolysis may be necessary. When systemic therapy is contraindicated or ineffective, catheter-directed therapy or surgical embolectomy might be considered.
4. Long-Term Management:
   After stabilization, a comprehensive diagnostic workup identifies risk factors, such as malignancy or inherited thrombophilia, informing secondary prevention strategies.

Broader Perspectives for Improved Patient Outcomes

While echocardiographic findings drive urgent decision-making, the integration of clinical context is paramount. In patients with cancer, there is an elevated risk for venous thromboembolism, necessitating a high index of suspicion for PE. Early recognition of McConnell’s sign, combined with an understanding of the patient’s comorbidities, can expedite life-saving interventions. Additionally, careful follow-up and consideration of inferior vena cava filters, long-term anticoagulation, and involvement of a multidisciplinary team (cardiology, pulmonology, hematology, and oncology) can improve patient outcomes.

Incorporating advanced imaging techniques, serial echocardiograms, and emerging biomarkers may further refine the diagnostic pathway. Further research and case studies offer insight into the nuanced interpretation of RV strain patterns, allowing for more targeted and individualized therapy.

References

• Alagna, G., MD (PGY1) & McCafferty, L., MD. (2024). Intern Ultrasound of the Month: A Sign of Acute Pulmonary Embolism. University Hospitals Emergency Medicine Residency. Retrieved from: https://www.thelandofem.com/blog/2024/2/26/iusotm-mcconnells-sign-pe
• McConnell MV, Solomon SD, Rayan ME, et al. (1996). Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol, 78(4), 469–473.
• Konstantinides SV, Meyer G, Becattini C, et al. (2019). ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). European Heart Journal, 41(4), 543–603.

This refined summary honors the original work, provides comprehensive echocardiographic and clinical context, and presents additional perspectives, aiding in the prompt recognition and management of acute PE.

Written on December 13th, 2024

Carotid Ultrasound Findings in a 47-Year-Old Patient (Written March 24, 2025)

1. Original Question and Responses

2. Explanation, Background, and Analysis

A carotid ultrasound evaluates blood flow in the common carotid artery (CCA), internal carotid artery (ICA), and external carotid artery (ECA). In this particular case, the patient’s CCA peak systolic velocity (PSV) is elevated (140 cm/s) on the right side, whereas the ICA-PSV is 80 cm/s. No plaque or significant intima-media thickening (IMT) is observed.

1. Key Carotid Ultrasound Parameters

   • Peak Systolic Velocity (PSV)
     • Represents the highest velocity of blood flow during systole (heart contraction).
     • Often compared against established normal ranges or thresholds to assess for possible stenosis.
   • Intima-Media Thickness (IMT)
     • Measures the combined thickness of the intima and media layers of the arterial wall.
     • Normal IMT usually indicates minimal atherosclerotic change, but does not fully exclude early disease.
   • PSV Ratios
     • PSV(ICA)/PSV(CCA) is a common index for evaluating the severity of stenosis.
     • Ratios ≥2 often indicate ≥50% ICA stenosis based on certain guidelines (e.g., NASCET).
   • Plaque Assessment
     • B-mode imaging visualizes atherosclerotic plaques or calcifications.
     • Absence of visible plaque greatly reduces the likelihood of significant obstruction.

2. Normal and Abnormal Ranges: PSV, IMT, and Ratios

   Carotid artery velocity and IMT values vary by age, sex, cardiovascular risk profile, and methodology. Table 1 provides approximate reference ranges and classifications for each major carotid segment (CCA, ICA, ECA), including possible differences by sex if reported in certain references. It is important to note that exact cutoffs differ among studies and clinical protocols.

   Parameter	Sex	Normal Range	Mild Abnormality	Moderate Abnormality	Severe Abnormality
   PSV (CCA) (cm/s)	M/F¹	~70–125 cm/s (20–60 yrs) IMT <0.9 mm²	125–140 cm/s	140–180 cm/s	>180 cm/s (especially if plaque present)
   PSV (ICA) (cm/s)	M/F¹	<125 cm/s (IMT <0.9 mm)	125–150 cm/s	150–200 cm/s	>200 cm/s (≥70% stenosis often suspected)
   PSV (ECA) (cm/s)	M/F¹	~60–120 cm/s (IMT <0.9 mm)	120–150 cm/s	150–200 cm/s	>200 cm/s (unusual unless significant disease exists)
   PSV Ratio PSV(ICA)/PSV(CCA)	M/F¹	<2.0 (suggesting <50% stenosis)	2.0–2.5 (possible ≥50% stenosis)	2.5–4.0 (often 60–70% stenosis)	>4.0 (≥70% stenosis likely)
   IMT (mm)	M/F¹	<0.9 mm	0.9–1.1 mm	1.1–1.4 mm	>1.4 mm (considered significantly abnormal)

3. NASCET Criteria and Additional Guidelines

   The North American Symptomatic Carotid Endarterectomy Trial (NASCET) established widely utilized benchmarks for carotid stenosis severity based on angiographic measurements. Ultrasound criteria (PSV, velocity ratios, presence of plaque) have been correlated with these angiographic findings. Frequently cited thresholds include:

   • ICA-PSV ≥125–130 cm/s for ≥50% stenosis
   • ICA-PSV ≥200–230 cm/s for ≥70% stenosis
   • PSV(ICA)/PSV(CCA) ≥2 often suggests ≥50% stenosis
   • PSV(ICA)/PSV(CCA) ≥4 often suggests ≥70% stenosis

   Below is an example summary table correlating Doppler velocity measurements with approximate NASCET-based stenosis grading:

   Stenosis Category (NASCET)	ICA-PSV (cm/s)	PSV(ICA)/PSV(CCA) Ratio	Approx. Luminal Narrowing
   <50%	<125 cm/s	<2.0	Minimal or no significant stenosis
   50–69%	125–230 cm/s	2.0–4.0	Moderate stenosis
   ≥70%	≥230 cm/s	≥4.0	Severe stenosis

   Clinical decisions often rely on Doppler ultrasound findings combined with plaque visualization, patient symptoms, and risk factor status. If ultrasound findings are equivocal or if the patient is symptomatic, additional imaging (CT/MR angiography) may be warranted.

4. Analysis for This Patient’s Findings

   1. Elevated Right CCA-PSV (140 cm/s)
      Slightly above general upper-normal limits. However, no plaque is identified, and IMT is not notably thick.
   2. Normal ICA-PSV (80 cm/s)
      • Well below the typical threshold of 125 cm/s that would suggest ≥50% stenosis.
      • PSV ratio (ICA/CCA) <1.0, far from the ≥2.0 cutoff for significant stenosis.
   3. Absence of Plaque
      Suggests that the high CCA velocity is not due to a focal stenosis or atherosclerosis.
   4. Possible Explanations
      • Hypertension or reduced arterial compliance could elevate flow velocity.
      • Technical Factors: Angle of insonation or sampling location can artificially elevate measured velocities.

5. Recommendations for Clinical Management

   1. Blood Pressure Optimization
      High systemic blood pressure can affect carotid velocities. Ensuring controlled blood pressure is crucial for vascular health.
   2. Risk Factor Modification
      Smoking cessation, lipid management, glycemic control, and a balanced diet can help prevent atherosclerotic progression.
   3. Periodic Ultrasound Follow-Up
      Repeat carotid ultrasound to monitor any changes in CCA-PSV, ICA-PSV, and IMT, especially if cardiovascular risk factors are present.
   4. Further Imaging if Warranted
      In cases of ambiguous ultrasound findings or symptomatic patients (e.g., transient ischemic attacks), CT/MR angiography may be considered to exclude significant stenosis definitively.

3. Detailed Analysis of This Patient’s Condition and Proposed Approach

Below is an expanded discussion that recaps the key question and the main responses (in English), followed by an analysis.

1. Recap of the Key Question (English)

   Question:
   A 47-year-old female patient has a right common carotid artery (CCA) peak systolic velocity (PSV) of 140 cm/s, while the right internal carotid artery (ICA) PSV is 80 cm/s. No plaque or significant intima-media thickening is seen. How should this elevated CCA velocity be interpreted?

2. Recap of the Main Responses (English)

   1. Response 1: Suggests that if the ICA velocity is normal, it might not be a significant issue. Possible explanations for elevated CCA velocity without plaque include severe hypertension or reduced arterial elasticity.
   2. Response 2: Briefly mentions that if the vessel looks thick, medication might help—implying that treatment could be aimed at addressing underlying risk factors.
   3. Response 3: References a standard guideline where PSV >125–130 cm/s and PSV(ICA)/PSV(CCA) ≥2 may indicate ≥50% stenosis.
   4. Response 4: Notes that elevated CCA PSV is not necessarily concerning if the ICA PSV is normal and IMT shows no abnormality.
   5. Response 5: Emphasizes that ICA velocity is the more critical parameter and a threshold of 125 cm/s for ICA PSV is often used to define >50% stenosis.

3. Analysis of the Responses and Proposed Approach

   • Since no plaque or significant intimal thickening is detected, and the ICA velocity (80 cm/s) is comfortably below the ≥125 cm/s threshold, there is no immediate ultrasound evidence of clinically significant stenosis.
   • The elevated CCA-PSV (140 cm/s) may reflect:
     • Underlying hypertension or arterial stiffness.
     • Technical factors during the ultrasound exam (e.g., Doppler angle or sampling error).
   • Because the ICA-PSV is well within normal limits, standard guidelines (including the NASCET-based criteria) do not support a diagnosis of >50% stenosis.
   • Management at this point primarily involves:
     • Ensuring blood pressure control and addressing other cardiovascular risk factors.
     • Follow-up ultrasounds to detect any emerging plaque or changes in velocity over time.
     • Further imaging (CT/MRA) only if new symptoms arise or if velocities/IMT significantly change in follow-up.
   • This approach aligns with the consensus in the responses: the normal ICA flow strongly suggests no hemodynamically significant stenosis at present.

In conclusion, the elevated CCA velocity alone—without plaque, abnormal IMT, or elevated ICA velocity—likely reflects a low-risk situation. Emphasis should be on general cardiovascular risk management and periodic follow-up, rather than invasive intervention.

References

1. Bluth EI, Ultrasound: A Practical Approach to Clinical Problems. Thieme Medical Publishers, 2008.
2. Grant EG, et al. Carotid Artery Stenosis: Gray-Scale and Doppler US Diagnosis—Society of Radiologists in Ultrasound Consensus Conference. Radiology 2003;229(2):340–346.
3. Barnett HJM, Taylor DW, Eliasziw M, et al. Benefit of Carotid Endarterectomy in Patients with Symptomatic Moderate or Severe Stenosis. N Engl J Med 1998;339(20):1415–1425.

Written on March 24, 2025

Ultrasound‑guided evaluation and management of elevated D‑dimer in a long‑term‑care resident (Written April 11, 2025)

Clinical vignette

An 85‑year‑old male resident of a long‑term‑care facility (LTCF) reported progressive exertional dyspnoea. Sputum culture yielded multidrug‑resistant Acinetobacter baumannii (MRAB). Previous episodes of hyperkalaemia had been managed conservatively. The facility possessed point‑of‑care ultrasound (POCUS) but lacked CT and MRI capability.

Three sets of plasma biomarkers were obtained over 48 h:

Values remained mildly but consistently above the upper reference limits for D‑dimer and NT‑proBNP, whereas renal clearance stayed preserved.

Sonographic armamentarium for an elevated D‑dimer

Reference values and graded abnormality thresholds

Abbreviations: RV – right ventricle; LV – left ventricle; TAPSE – tricuspid annular plane systolic excursion; S′ – tissue Doppler systolic velocity; PASP – pulmonary artery systolic pressure; IVC – inferior vena cava; RAP – right‑atrial pressure; S – systolic wave; D – diastolic wave.

Stepwise diagnostic algorithm in a sono‑only environment

Elevated D‑dimer  →  Clinical VTE probability score
                         │
           ┌─────────────┴─────────────┐
           │                           │
   Low / intermediate            High probability
       probability                      │
           │                           │
Compression venous duplex        Duplex + immediate TTE
           │                           │
    ┌──────┴──────┐              ┌─────┴─────┐
    │             │              │           │
Positive       Negative      RV strain   No RV strain
    │             │              │           │
Anticoag.   TTE + LUS        Treat as    LUS ± repeat
(see § 4)       │            presumptive    duplex
           ┌────┴────┐          PE
           │         │
        PE signs   No PE signs
           │         │
    Anticoag.   Re‑evaluate other

Management pathways based on sonographic findings

Guardian consent obtained for IRB-approved clinical research aimed at disseminating better clinical practices in hemodynamics.

Written on April 11, 2025

Interpretation of TTE findings in an 85-year-old gentleman (Written June 20, 2025)

An 85-year-old male underwent TTE to evaluate valvular and ventricular function. Normal reference limits follow contemporary recommendations from the American Society of Echocardiography (ASE), American College of Cardiology (ACC) and European Society of Cardiology (ESC).

1. Novisible thrombi in this study
2. Non-RHD:
suspicious severe AS & mild AR (I/IV) d/t senile sclerocalcified AV c LOM
(AVA=0.70/1.87cm2 by 2D/CE, AVAi=0.43cm2/m2 by 2D, Vmax=2.18m/s,
peak/meanPG=19/11mmHg, AV annulus=25.3mm, SVi=40.1ml/m2)
with post stenotic dilatation of ascending aorta=4.2cm
mild to moderate MS & mild MR (I/IV) d/t thickended MV c MAC
(MVA=1.21cm2 by 2D, MDPG=4.49mmHg)
2. Moderate global hypokinesia of LV
3. Enlarged LA (LAVI=58ml/m2) & RA sizes c reduced global LV systolic fx(EF=45%)
4. Moderate RVP (RVSP=58mmHg)
5. Mobile hyperechoic material(=0.58mm) at annulus of mitral valve
r/o calcium debris
6. indeterminate LV filling pattern

Findings and commentary

• 1. No visible thrombi in this study

  No intracardiac thrombus was visualised. Absence of left-atrial or left-ventricular thrombi is reassuring in an elderly individual with mildly reduced ejection fraction and probable diastolic dysfunction.

• 2. Non-RHD: suspicious severe AS & mild AR (I / IV) due to senile sclerocalcified aortic valve with limited opening motion (AVA = 0.70 / 1.87 cm² by 2-D / continuity, AVA_i = 0.43 cm² m^-2, V_max = 2.18 m s^-1, peak / mean ΔP = 19 / 11 mmHg, annulus 25.3 mm, SVI = 40.1 ml m^-2) with post-stenotic dilatation of the ascending aorta = 4.2 cm
  mild–moderate MS & mild MR (I / IV) due to thickened mitral valve with MAC (MVA = 1.21 cm² by 2-D, mean ΔP = 4.49 mmHg)

  Parameter	Patient	Normal / Guideline threshold	Interpretation
  Aortic Valve Area (2-D)	0.70 cm²	>1.0 cm² (severe < 1.0)	Meets anatomic criterion for severe AS
  AVA indexed (AVAi)	0.43 cm² m-2	>0.6 cm² m-2	Severe (low-flow state suspected)
  Vmax	2.18 m s-1	≥4.0 m s-1 severe	Only mild
  Mean ΔP	11 mmHg	≥40 mmHg severe	Only mild
  Stroke-volume index	40.1 ml m-2	35–65 ml m-2	Low-normal
  Ascending aorta	4.2 cm	<3.7 cm	Mild dilatation
  Mitral Valve Area	1.21 cm²	1.5–1.0 cm² moderate	Moderate MS
  Mean mitral gradient	4.5 mmHg	5–10 mmHg moderate	Low-moderate

  The discordance between a markedly reduced anatomic AVA (0.70 cm²) and a low gradient/velocity raises the possibility of low-flow, low-gradient aortic stenosis or technical under-measurement. Confirmation with Doppler calibration, a dobutamine stress-echo, or computed-tomography calcium scoring is advisable. :contentReference[oaicite:1]{index=1}

  Concomitant mild aortic regurgitation and moderate mitral stenosis, both degenerative in origin, compound the haemodynamic burden. Mild calcific mitral regurgitation (I/IV) is noted.

  Patient aortic-valve metrics versus guideline thresholds
  Parameter	Patient	Mild	Moderate	Severe
  Aortic valve area (AVA)	0.70 cm²	>1.5 cm²	1.0–1.5 cm²	<1.0 cm²
  AVA indexed (AVAi)	0.43 cm² m-2	>0.85 cm² m-2	0.6–0.85 cm² m-2	<0.6 cm² m-2
  Peak velocity (Vmax)	2.18 m s-1	2.0–2.9	3.0–3.9	≥4.0
  Mean pressure gradient	11 mmHg	<20	20–39	≥40

  The markedly reduced anatomic AVA with low gradient and velocity is discordant, suggesting low-flow, low-gradient aortic stenosis or technical under-measurement; confirmation with Doppler calibration, dobutamine stress-echo, or CT calcium scoring is advisable.

  Mitral-valve stenosis classification
  Parameter	Patient	Mild	Moderate	Severe
  Mitral valve area (MVA)	1.21 cm²	>1.5 cm²	1.0–1.5 cm²	≤1.0 cm²
  Mean pressure gradient	4.5 mmHg	<5 mmHg	5–10 mmHg	>10 mmHg

  Mild aortic regurgitation and mild degenerative mitral regurgitation (grade I / IV) accompany the stenotic lesions.

  Relevant equations

  • \( \displaystyle AVA = \frac{A_{\text{LVOT}} \times VTI_{\text{LVOT}}}{VTI_{\text{AV}}} \)
  • \( \displaystyle \Delta P = 4\,V^{2} \)
  • \( \displaystyle SV = A_{\text{LVOT}} \times VTI_{\text{LVOT}}, \;\; SVI = \dfrac{SV}{BSA} \)

• 3. Enlarged LA (LAVI = 58 ml m^-2) & RA sizes with reduced global LV systolic function (EF = 45 %)

  Parameter	Patient	Reference range	Interpretation
  Left-atrial volume index	58 ml m-2	16–34 ml m-2	Severely enlarged
  Ejection fraction (biplane)	45 %	53–73 %	Mildly reduced (global hypokinesia)

  Bi-atrial enlargement likely reflects chronic diastolic loading from valvular stenoses and longstanding pressure overload. The modestly reduced ejection fraction may represent after-load mismatch, myocardial degeneration, or concomitant coronary disease; careful clinical correlation is encouraged.

  Parameter	Patient	Normal	Mildly abnormal	Moderately abnormal	Severely abnormal
  LAVI (ml m-2)	58	<34	35-41	42-48	≥49
  Ejection fraction (%)	45	≥53	41-52	30-40	<30

  Marked bi-atrial dilation reflects chronic diastolic loading from valvular obstruction. The mildly reduced ejection fraction may relate to after-load mismatch, myocardial degeneration or concomitant coronary disease.

• 4. Moderate right-ventricular pressure (RVSP = 58 mmHg)

  RVSP (mmHg)	Classification
  <35	Normal
  35–44	Mild pulmonary hypertension
  45–59	Moderate pulmonary hypertension ← Patient
  ≥60	Severe pulmonary hypertension

  An RVSP of 58 mmHg falls within the moderate range and is most likely secondary to post-capillary (valvular and ventricular) pressure elevation. Right-heart catheterisation remains the reference standard where therapeutic decisions depend upon accurate pulmonary-vascular resistance.

• 5. Mobile hyperechoic material (0.58 mm) at the mitral annulus – rule-out calcium debris

  A small oscillating echo density along the calcified mitral annulus most often represents benign friable calcium or fibrin strands. Infective endocarditis is unlikely given the diminutive size (<1 cm) and absence of independent mobile stalk.

• 6. Indeterminate LV filling pattern

  Transmitral inflow and tissue-Doppler indices were insufficient to categorise diastolic filling. A restrictive or pseudonormal pattern may be masked by rhythm, loading conditions or Doppler alignment. Repeat echocardiography with complete diastolic assessment or cardiac MRI is recommended.

Guardian consent obtained for IRB-approved clinical research aimed at disseminating better clinical practices in hemodynamics.

Written on June 20, 2025

TTE findings and hemodynamic management in an elderly patient following traumatic subdural hemorrhage (Written July 11, 2025)

An 82-year-old male developed epilepsy after recovery from a traumatic subdural hemorrhage (T-SDH). Transthoracic echocardiography (TTE) performed during routine evaluation revealed ischemic myocardial injury and impaired ventricular function, prompting initiation of low-dose carvedilol for blood-pressure (BP) control.

TTE demonstrated an ischemic insult in the left anterior descending (LAD) coronary artery territory with moderate left-ventricular (LV) systolic dysfunction (left-ventricular ejection fraction = 43%); blood pressure was therefore managed with Dilatrend® 3.125 mg, half tablet.

Interpretation of key findings

• Ischemic insult in LAD territory frequently produces anterior-wall hypokinesia, limiting systolic performance and predisposing to heart-failure symptoms.
• LVEF = 43 % lies within the “heart-failure with mildly reduced ejection fraction” (HFmrEF) category, where neurohormonal blockade confers prognostic benefit.
• Moderate systolic dysfunction heightens vulnerability to afterload changes; gentle BP control is therefore warranted.

Rationale for carvedilol (Dilatrend®) 3.125 mg ½ tablet

1. Neurohormonal modulation. Carvedilol antagonises β₁, β₂, and α₁ receptors, attenuating the adrenergic drive that aggravates ischemia and LV remodeling.
2. Mortality benefit in ischemic cardiomyopathy. Clinical trials demonstrate reduced all-cause mortality and rehospitalisation when β-blockers are introduced at low dose and titrated upward in LV dysfunction.
3. Blood-pressure control with vasodilation. The additional α₁ blockade offers gentle peripheral vasodilation, lowering afterload without provoking reflex tachycardia.
4. Low starting dose for frailty. A half-tablet (≈ 1.56 mg) minimises initial bradycardia or hypotension in an elderly, potentially volume-sensitive patient recovering from intracranial pathology.

Suggested up-titration schedule^*

^*Dose escalation contingent on tolerance; slower titration advisable in orthostatic intolerance.

Clinical considerations

• Interaction with antiepileptic therapy: β-blockers rarely lower seizure threshold; careful observation remains prudent.
• Intracranial pressure (ICP): Abrupt hypotension may compromise cerebral perfusion after T-SDH; incremental dosing safeguards cerebral hemodynamics.
• Heart-failure management: Combine carvedilol with guideline-directed agents (e.g., ACE inhibitor, mineralocorticoid-receptor antagonist) as tolerated.
• Follow-up imaging: A repeat TTE at 3- to 6-month interval assists in tracking ventricular recovery or progression.

Guardian consent obtained for IRB-approved clinical research aimed at disseminating better clinical practices in hemodynamics.

Written on July 11, 2025

Transthoracic echocardiography assessment in a 92‑year‑old woman (Written July 29, 2025)

I. Patient background

• Age / Sex: 92‑year‑old female
• Comorbidities: end‑stage renal disease on maintenance hemodialysis, long‑standing hypertension, remote cold cerebrovascular accident

II. Quantitative echocardiographic findings

1. Normal sized cardiac chambers with normal global left‑ventricular systolic function (EF: 67 %).

2. Relaxation abnormality of LV filling pattern (E/e′: 14).

3. Moderate circumferential pericardial effusion without hemodynamic significance:
   • LV posterior: 1.62 cm
   • LV apex: 1.71 cm
   • RV side: 1.77 cm
   • RA side: 0.35 cm

4. Concentric left‑ventricular hypertrophy.

5. Slightly dilated sinus of Valsalva (36 mm) and ascending aorta (37 mm).

III. Guideline‑based evaluation

1. Left‑ventricular size and systolic function

   Parameter	Normal	Patient	Interpretation
   LVEF	≥ 53 % (women)	67 %	Normal
   LV internal dimensions / volumes	Within reference range	Normal by report	No dilation

2. Diastolic function  –  grading criteria

   Criterion	Grade				Patient
   	I (impaired relaxation)	II (pseudonormal)	III (restrictive, reversible)	IV (restrictive, fixed)
   E/A ratio	< 0.8	0.8–2.0	> 2.0	> 2.0	Not provided*
   Average E/e′	< 14	14–15	> 15	> 15	14
   Tricuspid regurgitation Vmax	< 2.8 m/s	> 2.8 m/s	> 2.8 m/s	> 2.8 m/s	Not provided
   LA volume index	< 34 mL/m²	> 34 mL/m²	> 34 mL/m²	> 34 mL/m²	Not provided

   • *Given the reported “relaxation abnormality” and borderline E/e′ of 14, the pattern is most compatible with Grade I (impaired relaxation) with borderline filling pressures.

3. Pericardial effusion size classification

   Maximum separation	Classification	Patient (RV side 1.77 cm)
   < 1.0 cm	Mild	Moderate
   1.0–2.0 cm	Moderate
   > 2.0 cm	Large

   No hemodynamic compromise is documented; therefore, tamponade physiology is absent.

4. Left‑ventricular hypertrophy (LVH)

   IVS / PW thickness	Normal	LVH threshold	Patient	Interpretation
   Posterior wall	< 1.0 cm (women)	≥ 1.1 cm	1.62 cm	Concentric LVH
   Interventricular septum*	< 1.0 cm	≥ 1.1 cm	Not provided

   • *Septal thickness was not included but concentric geometry is inferred from concentric wall thickening and preserved cavity size.
   
   

   Geometry pattern	Left ventricular mass index (LVMI)	Relative wall thickness (RWT)
   Normal geometry	Normal (< 95 g/m² in women, < 115 g/m² in men)	Normal (≤ 0.42)
   Concentric remodeling	Normal (< 95 g/m² in women, < 115 g/m² in men)	Increased (> 0.42)
   Concentric hypertrophy	Increased (≥ 95 g/m² in women, ≥ 115 g/m² in men)	Increased (> 0.42)
   Eccentric hypertrophy	Increased (≥ 95 g/m² in women, ≥ 115 g/m² in men)	Normal (≤ 0.42)

5. Aortic root and ascending aorta dimensions

   Segment	Upper normal (women, age > 40)	Patient	Interpretation
   Sinus of Valsalva	≤ 34 mm	36 mm	Slightly dilated
   Ascending aorta	≤ 35 mm	37 mm	Slightly dilated

IV. Integrated assessment

• The left ventricle demonstrates normal systolic performance with concentric hypertrophy, most likely secondary to long‑standing hypertension and chronic afterload burden associated with hemodialysis.
• Diastolic function is consistent with grade I impaired relaxation, while the E/e′ of 14 suggests borderline elevation of filling pressures; volume status fluctuations inherent to dialysis may influence these parameters.
• A moderate, circumferential pericardial effusion is present without hemodynamic significance; interval surveillance is warranted, particularly given the patient’s uremic milieu.
• The aortic root and proximal ascending aorta are mildly enlarged; dimensions are below thresholds generally considered for surgical or endovascular intervention at this age, yet serial imaging is prudent.

V. Clinical implications

1. Blood‑pressure optimization: Intensify antihypertensive strategy to limit further hypertrophic remodeling and aortic dilatation.
2. Volume management: Coordinate with dialysis team to achieve euvolemia, thereby reducing left‑atrial pressure and diastolic filling pressures.
3. Pericardial effusion monitoring: Repeat echocardiography if new symptoms (dyspnea, orthopnea, hypotension) occur or if an inflammatory etiology is suspected.
4. Serial aortic imaging: Consider annual echocardiographic or computed‑tomographic surveillance; expedite if growth > 3 mm appears within a year.
5. Comprehensive geriatric cardiac care: Continue multidisciplinary follow‑up focusing on frailty, cerebrovascular prevention, and dialysis‑related cardiovascular risk.

VI. Key teaching points

• In elderly dialysis patients, concentric LVH and grade I diastolic dysfunction are prevalent and portend heightened cardiovascular risk despite preserved LVEF.
• E/e′ values from 13–15 inhabit a gray zone; interpretation must integrate clinical volume status, atrial size, and pulmonary pressures.
• Pericardial effusion size alone does not dictate intervention; hemodynamic effect remains the critical determinant.
• Slight aortic dilatation in non‑Marfan, normotensive‑controlled elders is generally observed conservatively unless rapid expansion occurs.

Guardian consent obtained for IRB-approved clinical research aimed at disseminating better clinical practices in hemodynamics.

Written on July 29, 2025

Interpretation of Echocardiography Findings in a Clinical Case (Written September 7, 2025)

I. Case Echocardiography Report (English Translation)

Limited study due to supine position
Tachycardia (around 105 bpm)
Tracheostomy present

1. Grossly small LV cavity size with normal LV systolic function (LVEF = 60–65%).
2. Summation of E/A wave due to tachycardia.

• Poor acoustic window makes it difficult to compare accurately with the previous echocardiogram from May 23, 2023, but the LV cavity size appears reduced (42/29 mm then vs 37/26 mm now).

LVEDD: 36.8 mm
LVESD: 26.3 mm
IVSD: 9.5 mm
PWd: 9.4 mm
LA (AP dimension): 29.9 mm
PASP: 21.0 mmHg

II. Detailed Analysis of Echocardiographic Findings

Technical Limitations and Patient Condition

Limited study due to supine position
Tachycardia (around 105 bpm)
Tracheostomy present

The echocardiogram was technically limited by the patient's condition. The patient remained supine and had a tracheostomy in place, which likely impeded optimal positioning for transthoracic imaging. Additionally, the heart rate was elevated (~105 beats per minute), shortening the cardiac cycles. These factors contributed to suboptimal acoustic windows and reduced image quality, making the study less comprehensive than usual.

Left Ventricular Size and Systolic Function

Grossly small LV cavity size with normal LV systolic function (LVEF = 60–65%).

The study notes a markedly small left ventricular (LV) cavity, while the systolic function remains normal. LVEF (left ventricular ejection fraction) is approximately 60–65%, which falls within the normal range for adults, indicating preserved pumping ability. A small LV cavity size means the internal dimensions of the LV are on the lower end of normal or below normal. This could reflect the patient's body size, low blood volume, or dehydration, or a hyperdynamic state where the heart contracts vigorously. Importantly, despite the reduced chamber size, the normal ejection fraction suggests that the ventricular muscle contractility is intact and the stroke volume is maintained through compensatory mechanisms (such as the higher heart rate).

Diastolic Filling Pattern (E/A Wave)

Summation of E/A wave due to tachycardia.

The report indicates that the early (E) and atrial (A) filling waves on transmitral Doppler have merged into a single summation wave. This is attributable to the tachycardia: at a heart rate of ~105 bpm, the diastolic filling period is so short that the normal two distinct filling phases (early passive filling and late atrial contraction filling) overlap. As a result, it is challenging to separate E and A waves, making it difficult to assess diastolic function in the usual way. Under normal conditions (with lower heart rates), the E/A ratio is evaluated to gauge diastolic function. In this patient, because of E–A fusion, a reliable E/A ratio could not be obtained. It is therefore not possible to determine the diastolic dysfunction grade from this study. For reference, in an adult heart at normal heart rates, an E/A ratio around 1–1.5 is expected in normal diastolic function, whereas values significantly below or above that range suggest diastolic dysfunction (Grade I, II, or III as shown below).

Table: Grading of Left Ventricular Diastolic Dysfunction (Adults)

Comparison with Previous Study

Poor acoustic window makes it difficult to compare accurately with the previous echocardiogram from May 23, 2023, but the LV cavity size appears reduced (42/29 mm then vs 37/26 mm now).

The report compares the current findings with a prior echocardiographic study (performed on May 23, 2023). Due to the poor imaging quality of the current study, an exact side-by-side comparison is limited. However, it is noted that the left ventricular cavity dimensions have decreased since the previous exam. Previously, the LV end-diastolic dimension (LVEDD) and end-systolic dimension (LVESD) were approximately 42 mm and 29 mm, respectively. In the current study, these measurements are about 37 mm (LVEDD) and 26 mm (LVESD). Such a reduction in chamber size over time could be influenced by differences in volume status, measurement technique, or patient condition between the two exams. In a stable clinical scenario, a significantly smaller LV cavity now might suggest the patient has a lower circulating volume or higher sympathetic tone at the time of the exam. It is also possible that the previous study had more optimal imaging, and the current measurements underestimated the true size due to suboptimal visualization.

Other Quantitative Measurements

LVEDD: 36.8 mm
LVESD: 26.3 mm
IVSD: 9.5 mm
PWd: 9.4 mm
LA (AP dimension): 29.9 mm
PASP: 21.0 mmHg

The table below summarizes the key echocardiographic measurements for this patient and compares them to normal adult reference ranges:

As shown above, the patient's cardiac dimensions and pressures are mostly within normal limits, aside from the notably small LV cavity size. The LVEDD is below the typical normal range even for a female patient, which aligns with the qualitative observation of a small LV cavity. The ventricular wall thicknesses (IVS and PW) are in the normal range, indicating no LV hypertrophy. The left atrial size is normal (not enlarged), and the estimated pulmonary artery systolic pressure is also normal, suggesting no evidence of pulmonary hypertension. Overall, aside from the reduced LV chamber size, there are no abnormal structural findings.

III. Clinical Implications and Next Steps

In summary, this echocardiographic evaluation reveals a small left ventricular cavity with preserved systolic function and indeterminate diastolic function due to tachycardia. These findings must be interpreted in the context of the patient's clinical state. Below are possible contributing factors for these echo findings and recommended subsequent steps in management and evaluation.

Potential Contributing Factors

• Low preload or volume status: The small LV dimensions may reflect decreased filling of the heart, as seen with intravascular volume depletion (e.g., dehydration or aggressive diuresis). When the body’s volume status is low, the LV appears smaller because it is not filled to normal capacity.
• Tachycardia: The elevated heart rate shortens diastolic filling time, inherently limiting how much blood the LV can accommodate at end-diastole. This leads to smaller measured LV cavity sizes. The tachycardia also caused the fusion of E and A waves, preventing a standard assessment of diastolic function.
• High contractility (hyperdynamic state): If the patient is in a hyperdynamic circulatory state (for example, due to stress, sepsis, pain, or use of inotropic medications), the heart can contract more vigorously, which often results in a smaller end-systolic dimension and can give the appearance of a very small LV cavity on echocardiography.
• Measurement or imaging factors: Given the suboptimal acoustic window, there is a possibility that the true LV size is slightly larger than measured. Poor visualization can lead to underestimation of chamber dimensions. However, the consistency of measurements and overall appearance still suggest a genuinely small LV in this case.

Recommended Next Steps

• Optimize volume status if needed: Correlate the echocardiographic findings with clinical signs of volume status. If the patient appears volume-depleted (e.g., hypotensive, low jugular venous pressure, poor skin turgor), cautiously increasing intravascular volume (fluid administration) may be considered to see if it leads to improved hemodynamics and possibly a more normal LV size on a follow-up assessment.
• Address the tachycardia: Investigate and manage the cause of the elevated heart rate. If appropriate, rate control (using medications or treating underlying triggers such as pain, agitation, or fever) could be beneficial. Slowing the heart rate would prolong diastolic filling time, which not only can improve the patient’s cardiac output if stroke volume is limited by filling, but also would allow a clearer assessment of diastolic function (separating the E and A waves on Doppler).
• Repeat imaging under better conditions: Once the patient’s condition allows, a repeat transthoracic echocardiogram in a better setting (for instance, with the patient in the left lateral decubitus position to enhance imaging windows and at a controlled heart rate) is advisable. If transthoracic windows remain poor and detailed information is needed, a transesophageal echocardiogram (TEE) could be performed for clearer images. A follow-up study could confirm whether the small LV cavity was transient (due to reversible factors like tachycardia or low volume) or persistent.
• Continue standard care and monitoring: Given that systolic function is normal and there are no signs of elevated filling pressures or pulmonary hypertension, the primary focus should remain on the patient’s overall clinical management. The heart appears structurally and functionally adequate in this study. Ongoing monitoring of cardiac function can be done as needed, especially if there are changes in clinical status. If any new symptoms or signs of cardiac dysfunction arise, further detailed cardiac evaluation should be undertaken.

Written on September 7, 2025

Echocardiographic Findings of Multichamber Enlargement and Pulmonary Hypertension (Written September 7, 2025)

I. Introduction

The following report presents an adult patient’s echocardiographic findings, which are notable for multiple chamber enlargements, preserved left ventricular systolic function, and evidence of pulmonary hypertension. It is written as a case study for a clinical audience ranging from medical trainees to experienced cardiologists. This report will translate the key echocardiography results from the original Korean report into English and provide a detailed interpretation of each finding. No identifiable patient information is included, and the discussion is focused on understanding the clinical significance of the findings, reviewing normal reference ranges (for adults), and outlining the differential diagnosis and recommended next steps in management.

II. Summary of Echocardiographic Findings

1. Enlarged LA (LAVI: 87 mL/m²) with normal global LV systolic function (EF: 70%).
2. Enlarged RA and RV with mildly reduced RV systolic function (FAC: 33%).
3. Moderate pulmonary hypertension (RVSP: 57 mmHg) with IVC plethora (25 mm).
4. Elevated LV filling pressure (E/e′: 13).
5. At least moderate TR (grade II–III/IV) with dilated TV annulus (45 mm) and slightly thickened leaflet.
6. Concentric remodeling of LV.
7. Dilated sinus of Valsalva (39 mm) and ascending aorta (36 mm).

In summary, the echocardiogram (transthoracic echocardiography) reveals severe left atrial enlargement, biatrial and right ventricular enlargement, preserved left ventricular ejection fraction, mild right ventricular systolic dysfunction, and evidence of moderate pulmonary hypertension. Notably, there is significant tricuspid regurgitation with annular dilatation, and the left ventricle shows concentric remodeling consistent with long-standing pressure load. The aortic root is mildly dilated. Table 1 below provides key measurements compared to normal adult reference ranges for clarity:

^*FAC: Fractional Area Change (measurement of RV systolic function)

III. Detailed Interpretation of Findings

A. Left Atrial Enlargement and LV Systolic Function

1. Enlarged LA (LAVI: 87 mL/m²) with normal global LV systolic function (EF: 70%).

The left atrium (LA) is markedly enlarged, as indicated by a left atrial volume index (LAVI) of 87 mL/m². In adults, normal LAVI is ≤ 34 mL/m²; thus, this value represents severe LA enlargement. Such a large LA volume usually reflects chronically elevated left atrial pressure over time, often due to longstanding diastolic dysfunction or other causes of impaired filling. The consequence of severe LA enlargement is significant because it predisposes to atrial fibrillation and other atrial arrhythmias. Despite this enlargement, the left ventricular (LV) ejection fraction is 70%, which is within normal to high-normal range, indicating preserved global LV systolic function. In other words, the pumping ability of the LV is intact, suggesting that the patient’s issues are not due to systolic heart failure but more likely related to diastolic function (filling of the heart). A normal EF with a large LA strongly points toward heart failure with preserved ejection fraction (HFpEF), where the heart’s relaxation is abnormal. It is also worth noting that an EF of 70% can be seen in hyperdynamic states or simply as the upper end of normal; in this context, it confirms that systolic function is not impaired.

B. Right Atrium and Right Ventricle Enlargement; RV Function

2. Enlarged RA and RV with mildly reduced RV systolic function (FAC: 33%).

Both the right atrium (RA) and right ventricle (RV) are enlarged. In a normal adult heart, the RA area is usually less than ~18 cm², and the RV’s basal dimension is typically under 42 mm. Although exact measurements are not listed here, the qualitative description indicates the dimensions exceed those normal limits. RV enlargement often accompanies chronic pressure or volume overload of the right heart. In this case, a likely reason is the elevated pressure in the pulmonary circulation (discussed below) causing strain on the RV, and significant tricuspid regurgitation causing volume overload of the RA.

The RV systolic function is reported as mildly reduced, with a fractional area change (FAC) of 33%. FAC is a percentage that measures how much the RV area decreases from diastole to systole; a normal RV FAC is ≥ 35%. Thus, 33% represents a slight reduction in RV contractile performance. Mild RV dysfunction in the presence of RV dilation suggests that the RV is starting to struggle against increased afterload (pressure in the pulmonary artery) or volume load. However, the dysfunction is only mild at this stage, which means the RV is still compensating relatively well. Monitoring RV function is important, because progressive pulmonary hypertension or ongoing volume overload can further impair the RV over time.

C. Pulmonary Hypertension and IVC Plethora

3. Moderate pulmonary hypertension (RVSP: 57 mmHg) with IVC plethora (25 mm).

The estimated right ventricular systolic pressure (RVSP) is 57 mmHg, which indicates pulmonary hypertension (PH). By echocardiographic criteria, an RVSP above approximately 50 mmHg falls into the moderate range of pulmonary hypertension. (For reference, normal RVSP is typically < 35 mmHg, and values of 35–50 mmHg suggest mild PH, while values above ~50–60 mmHg indicate at least moderate PH.) This RVSP is derived from the tricuspid regurgitation jet velocity on Doppler echocardiography using the modified Bernoulli equation, plus an estimate of right atrial pressure. In this case, the inferior vena cava (IVC) is dilated to 25 mm and noted to be plethoric (full and with poor collapse), which suggests an elevated RA pressure (often ~15 mmHg). The dilated, non-collapsing IVC is an important ancillary sign supporting the presence of pulmonary hypertension and right heart strain. An elevated RA pressure is often seen when there is chronic pressure overload on the right side of the heart.

Moderate pulmonary hypertension in this patient is likely a consequence of left heart pathology (post-capillary pulmonary hypertension). The severely enlarged LA and elevated filling pressures (see finding D) raise pressure in the pulmonary veins, which transmits back to the pulmonary artery, causing increased pulmonary artery pressure. This is known as Group II pulmonary hypertension (pulmonary hypertension secondary to left heart disease). The presence of PH has significant clinical implications: it increases workload on the RV, can lead to symptoms like shortness of breath, and requires investigation into reversible causes or direct management of the underlying cause (in this case, treating the left heart dysfunction). Confirmation of the severity and type of pulmonary hypertension can be pursued with a diagnostic right heart catheterization if needed.

D. Elevated Left Ventricular Filling Pressure (Diastolic Dysfunction)

4. Elevated LV filling pressure (E/e′: 13).

The ratio of early mitral inflow velocity to mitral annular early diastolic velocity (E/e′) is 13. This Doppler index is used to estimate left ventricular filling pressures (i.e., pressure in the left atrium during diastole). In general, an E/e′ ratio above 14 is considered indicative of elevated LV filling pressure, while values between about 8 and 12 are borderline or inconclusive by themselves. An E/e′ of 13 is at the high end of borderline, and given the context of markedly enlarged LA and other echocardiographic features, it strongly suggests that the patient has elevated left-sided filling pressures. In simpler terms, the pressure in the left heart when the ventricle is relaxing is higher than normal.

This finding is consistent with diastolic dysfunction of the LV. When the LV has impaired relaxation or reduced compliance (stiffness), it leads to higher pressure for any given volume of filling, which then transmits to the left atrium. The combination of this E/e′ ratio with the LA enlargement and the tricuspid regurgitation velocity (which contributes to the RVSP) points to at least moderate diastolic dysfunction (often categorized as Grade II diastolic dysfunction, or “pseudonormal” filling pattern, if mitral inflow patterns were analyzed). Essentially, the heart’s filling phase is impaired, corroborating the diagnosis of HFpEF (heart failure with preserved ejection fraction). Recognizing elevated filling pressures is crucial, as it guides therapy (e.g., diuretics, blood pressure control) and helps explain symptoms like exercise intolerance or dyspnea even though EF is preserved.

E. Tricuspid Regurgitation and Tricuspid Valve Changes

5. At least moderate TR (grade II–III/IV) with dilated TV annulus (45 mm) and slightly thickened leaflet.

The echocardiogram indicates at least moderate tricuspid regurgitation (TR), graded roughly as II–III on a scale where I is mild and IV is severe. Moderate TR means a significant amount of blood is leaking back through the tricuspid valve from the right ventricle to the right atrium during systole. The tricuspid valve (TV) annulus is measured at 45 mm, which is dilated well beyond normal. (Typically, a normal tricuspid annulus diameter is around 28–35 mm in adults; an annulus > 40 mm is clearly enlarged.) A dilated annulus often accompanies significant TR, since the valve leaflets can no longer coapt fully when the ring is enlarged. The mention of a slightly thickened leaflet suggests there are some structural changes to the valve leaflets (which could be due to age-related degeneration or other pathology), but no gross malformation is noted.

These findings together point toward functional (secondary) TR rather than primary valvular disease. In functional TR, the valve itself is essentially normal but becomes incompetent due to dilation of the annulus and distortion of the valve geometry, usually from right atrial and right ventricular enlargement. The most common cause for this scenario is pulmonary hypertension or left heart failure leading to volume overload in the right heart. Here, the moderate TR is likely a consequence of the elevated pulmonary pressures (and consequent RV enlargement) discussed above. Moderate TR can contribute to further RA enlargement and signs of systemic venous congestion (like liver congestion or edema) if severe enough. It is an important finding because if TR becomes severe, it can lead to significant morbidity, and interventions (such as surgical tricuspid valve repair or newer catheter-based treatments) might be considered. At the moderate stage, management focuses on treating the underlying cause (reducing pulmonary pressures and venous congestion) and observing if the regurgitation progresses.

F. Concentric LV Remodeling

6. Concentric remodeling of LV.

The left ventricle is described as having “concentric remodeling.” This term indicates that the LV walls are relatively thickened (or the chamber radius is relatively small) without a significant increase in overall LV mass beyond normal. In concentric remodeling, the wall thickness increases as an adaptation to pressure overload, but the LV cavity size is normal and muscle mass is not excessively enlarged (distinguishing it from concentric hypertrophy, where there is an increase in muscle mass as well). This pattern is commonly seen in patients with long-standing hypertension or other conditions that impose chronic pressure load on the heart. Essentially, the heart muscle thickens to make the wall stronger to pump against high pressure.

Concentric remodeling is consistent with the patient’s other findings that suggest hypertensive heart disease. It contributes to diastolic dysfunction because a thicker, less compliant ventricle relaxes and fills less easily. Along with the elevated filling pressures and LA enlargement, the concentric remodeling of the LV further supports the idea that the patient’s cardiac changes are due to chronic pressure overload (likely high blood pressure over time). Management of a patient with concentric remodeling focuses on aggressive control of blood pressure and other risk factors to prevent progression to heart failure or overt LV hypertrophy.

G. Dilated Aortic Root (Sinus of Valsalva) and Ascending Aorta

7. Dilated sinus of Valsalva (39 mm) and ascending aorta (36 mm).

The sinus of Valsalva (the aortic root just above the aortic valve) measures 39 mm, and the ascending aorta measures 36 mm in diameter. These values are mildly elevated above normal expectations for an adult (typical normal upper limits for the aortic root are in the mid-30s millimeter range, varying with age and body size). While different guidelines have slightly different cutoff values, generally an aortic root diameter of around 40 mm or more would be considered dilated. In this case, 39 mm is at the borderline of mild dilatation, and 36 mm in the ascending aorta is also slightly enlarged.

Mild dilation of the aortic root and ascending aorta can be associated with long-standing hypertension (which can cause the aorta to enlarge over time due to the constant high pressure load on the vessel wall). Other causes can include connective tissue disorders (like Marfan syndrome or bicuspid aortic valve with aortopathy), but those typically cause larger degrees of dilation and often at younger ages. There is no indication from the echocardiogram of any aortic valve dysfunction, and the dilation is modest. The clinical approach to a mildly dilated aorta is to ensure optimal blood pressure control and to follow the aortic dimensions over time with serial imaging. Usually, no surgical intervention is indicated until the diameter is significantly larger (for example, ≥ 45–50 mm depending on patient-specific factors and guidelines). Thus, these findings serve as a reminder to manage risk factors and plan follow-up imaging to monitor the aorta for any further enlargement.

IV. Synthesis and Differential Diagnosis

When integrating all of these echocardiographic findings, a unifying theme emerges: the heart shows changes consistent with long-standing pressure overload and diastolic dysfunction, with secondary effects on the right heart. The severe left atrial enlargement, elevated filling pressure, and concentric LV remodeling point strongly toward a chronic hypertensive heart disease picture leading to heart failure with preserved ejection fraction (HFpEF). In HFpEF caused by hypertension (or similar conditions), the thickened LV walls and stiffness elevate the pressure in the left ventricle during diastole, which in turn raises left atrial pressure and causes the left atrium to enlarge markedly. The elevated left-sided pressures transmit to the pulmonary circulation, causing pulmonary hypertension. As a result, the right ventricle faces increased resistance and gradually dilates and weakens slightly, and the tricuspid valve annulus stretches, leading to functional tricuspid regurgitation and right atrial enlargement.

Normative and Pathological Values for Severity Classifications

Normative Values Across the Lifespan from Neonates to Adults

This section presents a peer-reviewed compilation of normative values for echocardiographic measurements, spanning neonates, pediatric patients, and adults. It serves as a critical reference for clinicians, ensuring accurate interpretation of echocardiographic data across different age groups and enhancing diagnostic precision in various clinical scenarios.

Echocardiography Study Notes for Quick Reminder

This quick reference guide provides a synthesized overview of key echocardiography concepts, focusing on the relationship between echocardiographic findings and underlying pathophysiological mechanisms. Designed to aid in the comprehensive assessment and management of cardiovascular conditions, it highlights how specific echocardiographic results correlate with various cardiac pathologies. Drawn from my personal study notes, this summary serves as a helpful reminder of essential materials, though I cannot guarantee the absolute accuracy of these notes.

(A) Right Ventricle

(B) Right Atrium

(C) Diastolic Dysfunction and Left Atrium

(E) Surgical Indications

(F) Other Diseases

A Collection of Readings on Hemodynamics, for Echocardiography

(A) Dynamics of the Vascular System: Interaction with Heart (2nd edition), by John K-J Li

This foundational text explores the intricate dynamics of the vascular system and its interaction with the heart, offering a detailed understanding of hemodynamic principles. The book emphasizes the physiological and mechanical aspects of blood flow and pressure, and their implications for cardiac function, providing essential knowledge for those studying or practicing echocardiography.