A Systematic Approach to Interpreting Echocardiography Reports: Ten Essential Steps for the Internist
A Systematic Approach to Interpreting Echocardiography Reports: Ten Essential Steps for the Internist
Abstract
Echocardiography remains the cornerstone of cardiovascular assessment in internal medicine practice. However, the complexity of modern echocardiographic reports can be daunting for non-cardiologists. This review provides a structured, ten-step approach to interpreting echocardiography reports, emphasizing practical pearls for internists and highlighting common pitfalls that can lead to clinical errors. By mastering this systematic framework, clinicians can extract critical information efficiently, recognize patterns of disease, and make informed management decisions.
Introduction
Transthoracic echocardiography (TTE) has evolved from a simple imaging modality to a comprehensive hemodynamic assessment tool. Contemporary reports incorporate M-mode, two-dimensional, Doppler, strain imaging, and three-dimensional data, generating extensive quantitative and qualitative information. For the busy internist, efficiently extracting clinically relevant data while avoiding misinterpretation is crucial. This ten-step approach provides a roadmap for systematic report analysis, applicable across diverse clinical scenarios from acute dyspnea to pre-operative assessment.
Step 1: Verify Patient Identity and Clinical Context
The Foundation of Interpretation
Begin by confirming patient demographics and the indication for the study. This seemingly obvious step prevents catastrophic errors when multiple studies exist in the electronic record. Note the study date—serial echocardiograms require chronological interpretation.
Pearl: Always correlate the clinical indication with your specific question. A study ordered for "chest pain" may not adequately assess for endocarditis if that diagnosis was considered after the study was performed.
Oyster: The quality of echocardiographic interpretation heavily depends on the clinical information provided. Studies ordered with vague indications like "abnormal ECG" yield less focused reports than those with specific questions such as "rule out pericardial effusion in lupus patient."
Step 2: Assess Image Quality and Technical Adequacy
Review the technical quality statement, typically found in the report's opening. Terms like "limited acoustic windows," "technically difficult study," or "suboptimal images" should raise caution flags.
Hack: When image quality is suboptimal, focus on the most reliably visualized structures. The apical four-chamber view is usually best visualized, making it reliable for left ventricular size assessment and mitral valve pathology even when parasternal views are limited.(1)
Poor acoustic windows are common in patients with obesity, chronic obstructive pulmonary disease, or mechanical ventilation. In such cases, consider whether transesophageal echocardiography or cardiac MRI might be necessary for definitive assessment.
Step 3: Evaluate Left Ventricular Size and Systolic Function
Left Ventricular Ejection Fraction (LVEF): Beyond the Single Number
LVEF is often the first value clinicians seek, but context is essential. Normal LVEF ranges from 52-72% (males) and 54-74% (females) by Simpson's biplane method.(2) However, several nuances deserve attention:
Pearl: LVEF can be "normal" despite significant systolic dysfunction in several scenarios:
- Early dilated cardiomyopathy with preserved contractility but increased chamber size
- Regional wall motion abnormalities with compensatory hyperkinesis elsewhere
- High afterload states (severe hypertension) masking underlying dysfunction
Oyster: Beware of falsely elevated LVEF in small, hypertrophied ventricles (hypertrophic cardiomyopathy) or falsely reduced LVEF in dilated ventricles with preserved stroke volume. Always correlate with left ventricular dimensions.
Hack: When LVEF reports seem discordant with clinical presentation, look for qualitative descriptions of wall motion. Terms like "global hypokinesis" with LVEF 50-55% suggest early cardiomyopathy requiring close follow-up, even though the number appears "normal."
Left ventricular end-diastolic diameter (LVEDD) and end-systolic diameter (LVESD) provide crucial context. Normal LVEDD is <5.8 cm (males) and <5.2 cm (females).(2) Dilated cardiomyopathy shows both reduced LVEF and increased LVEDD, while restrictive cardiomyopathy may show reduced LVEF with normal or small LVEDD.
Step 4: Assess Regional Wall Motion Abnormalities
The left ventricle is divided into 17 segments corresponding to coronary artery territories.(3) Wall motion is graded as normal, hypokinetic (reduced thickening), akinetic (absent thickening), or dyskinetic (paradoxical outward motion).
Pearl: The distribution of wall motion abnormalities suggests etiology:
- Single coronary territory: Ischemia or infarction
- Multiple non-contiguous territories: Embolic events
- Global hypokinesis with apical sparing: Cardiac amyloidosis
- Apical ballooning with basal hyperkinesis: Takotsubo cardiomyopathy
Hack: Calculate the wall motion score index (WMSI) if not provided: sum of segment scores divided by number of segments visualized. WMSI >1.7 predicts adverse outcomes post-myocardial infarction.(4)
Step 5: Evaluate Diastolic Function
The Forgotten Half of the Cardiac Cycle
Diastolic dysfunction is present in approximately 50% of heart failure patients and portends worse prognosis even when LVEF is preserved.(5) Modern guidelines use an integrated approach combining multiple parameters:
Key parameters include:
- E/A ratio (early to late mitral inflow velocity)
- E/e' ratio (mitral inflow to tissue Doppler)
- Left atrial volume index (LAVI)
- Tricuspid regurgitation velocity
Pearl: Diastolic function grading:
- Grade I (impaired relaxation): E/A <0.8, E/e' <8, normal LA size
- Grade II (pseudonormal): E/A 0.8-2.0, E/e' 9-12, mildly dilated LA
- Grade III (restrictive): E/A >2, E/e' >13, severely dilated LA
Oyster: E/A ratio reverses to "pseudonormal" in moderate diastolic dysfunction, masquerading as normal. Always check E/e' ratio and left atrial size to avoid missing significant diastolic dysfunction.
Hack: In atrial fibrillation, E/A ratio is unreliable. Focus on E/e' ratio (average of septal and lateral e') and LAVI. An E/e' >14 strongly suggests elevated filling pressures regardless of rhythm.(6)
Step 6: Analyze Left Atrial Size
Left atrial enlargement reflects chronic elevation of left ventricular filling pressures and predicts atrial fibrillation, stroke, and mortality. Normal LAVI is <34 mL/m² for both genders.(2)
Pearl: Progressive LA enlargement over serial studies indicates inadequate control of underlying pathology (hypertension, valvular disease, or diastolic dysfunction) even if symptoms haven't worsened.
Hack: When LAVI is not reported but LA diameter is given, use this approximation: LA diameter >4.0 cm suggests clinically significant enlargement and warrants attention to diastolic function and atrial fibrillation risk.
Step 7: Assess Valvular Function
A Structured Valve-by-Valve Approach
For each valve, assess structure, motion, stenosis severity, and regurgitation severity.
Mitral Valve: Mitral stenosis severity is defined by valve area: severe <1.0 cm², moderate 1.0-1.5 cm², mild >1.5 cm². Mean gradient >10 mmHg indicates severe stenosis.
Mitral regurgitation (MR) grading uses multiple parameters. Effective regurgitant orifice area (EROA) >0.40 cm² or regurgitant volume >60 mL defines severe MR.(7)
Pearl: Distinguish primary (organic) from secondary (functional) MR. Primary MR shows structural leaflet abnormalities (prolapse, flail, rheumatic thickening). Secondary MR occurs with structurally normal leaflets but annular dilatation or papillary muscle displacement from LV remodeling.
Aortic Valve: Severe aortic stenosis (AS) is defined by valve area <1.0 cm², mean gradient >40 mmHg, or peak velocity >4.0 m/s.(8) However, low-gradient AS presents challenges.
Oyster: In low-flow, low-gradient AS with reduced LVEF, valve area may appear severe but gradients are low due to poor LV function. Dobutamine stress echo helps distinguish true severe AS from pseudo-severe AS. True severe AS shows minimal change in valve area despite increased flow.
Pearl: Aortic sclerosis (thickening without stenosis) is common in elderly patients and doesn't require intervention but indicates atherosclerotic risk.
Tricuspid Valve: Tricuspid regurgitation (TR) is often underappreciated. Severe TR (EROA >0.40 cm²) leads to right heart failure and requires attention, especially before left-sided valve surgery.
Hack: Tricuspid regurgitation velocity allows non-invasive estimation of pulmonary artery systolic pressure (PASP): PASP = 4V² + right atrial pressure (typically estimated as 5-10 mmHg). Velocity >2.8 m/s suggests pulmonary hypertension (PASP >35 mmHg).
Step 8: Evaluate Right Ventricular Function and Pulmonary Pressures
The right ventricle (RV) is often overlooked but critical in conditions like pulmonary embolism, pulmonary hypertension, and heart failure.
Pearl: Normal RV is smaller than LV in apical four-chamber view (RV:LV ratio <0.6). When RV appears as large or larger than LV, suspect RV enlargement from volume overload (atrial septal defect, TR) or pressure overload (pulmonary hypertension).
RV systolic function is assessed by:
- TAPSE (tricuspid annular plane systolic excursion): Normal >17 mm
- RV S' (tissue Doppler velocity): Normal >9.5 cm/s
- RV fractional area change: Normal >35%
Oyster: Isolated TAPSE reduction may occur with septal infarction affecting RV longitudinal function despite normal RV contractility. Look for corroborative findings.
Hack: The "60/60 sign" in acute pulmonary embolism: RV systolic pressure <60 mmHg with RV acceleration time <60 ms suggests proximal PE with acute RV dysfunction.
Pulmonary hypertension is classified as:
- Mild: PASP 36-45 mmHg
- Moderate: PASP 46-60 mmHg
- Severe: PASP >60 mmHg
Step 9: Examine the Pericardium
Pericardial effusion size is graded as:
- Small: Echo-free space <10 mm
- Moderate: 10-20 mm
- Large: >20 mm
Pearl: Size doesn't equal hemodynamic significance. Rapidly accumulating small effusions cause tamponade, while slowly accumulating large effusions may be asymptomatic.
Signs of tamponade physiology include:
- Right atrial and RV diastolic collapse
- Respiratory variation in mitral inflow >25% and tricuspid inflow >40%
- Inferior vena cava plethora with absent respiratory collapse
Hack: In loculated effusions post-cardiac surgery, routine signs may be absent. Look for chamber compression regardless of location.
Pericardial thickening (>3 mm) with restrictive physiology suggests constrictive pericarditis, requiring differentiation from restrictive cardiomyopathy—often challenging and requiring advanced imaging or catheterization.
Step 10: Look for Incidental but Important Findings
The Details That Matter
Don't overlook incidental findings that may have major clinical implications:
Pearl: Intracardiac masses require characterization:
- Mobile, pedunculated masses on valves: Endocarditis vegetations or fibroelastomas
- Left atrial masses: Thrombus (especially in atrial fibrillation) vs. myxoma
- Ventricular masses: Thrombus vs. tumor
Thrombus identification requires:
- Documented reduced LVEF or regional akinesis for LV thrombus
- Atrial fibrillation or mitral stenosis for LA thrombus
- Distinct margins and independent motion
Oyster: Artifacts mimicking masses are common, especially near the mitral valve annulus and atrial septum. If uncertain, transesophageal echo or cardiac MRI provides definitive assessment.
Incidental valve vegetations, patent foramen ovale (PFO), or atrial septal aneurysms may explain cryptogenic stroke. Aortic atheroma >4 mm is an embolic source.
Hack: Always check the aortic root diameter, especially in young patients with aortic regurgitation or bicuspid aortic valve. Aortic root >4.0 cm warrants surveillance imaging and genetic evaluation for connective tissue disorders.
Integrating Echo Findings with Clinical Context
After completing these ten steps systematically, synthesize findings into a coherent clinical picture. Ask:
- Do the findings explain the patient's symptoms?
- Are there unexpected findings requiring attention?
- Are serial changes significant (compare with previous studies)?
- What additional testing might be needed?
- Does this change management?
Pearl: When echo findings conflict with clinical presentation, consider:
- Technical limitations requiring repeat study
- Wrong diagnosis being pursued
- Additional testing needed (stress echo, TEE, cardiac MRI, catheterization)
Common Pitfalls to Avoid
- Over-relying on LVEF alone without considering chamber size, diastolic function, and wall motion pattern
- Dismissing "trace" or "mild" valvular regurgitation without ensuring it's truly trivial (trace TR/MR is nearly universal and normal)
- Ignoring right heart assessment in unexplained dyspnea
- Missing low-gradient aortic stenosis in patients with symptoms but "only moderate" gradients
- Failing to recognize cardiac amyloidosis patterns (increased wall thickness, low voltage ECG, apical sparing strain pattern)
Conclusion
Systematic interpretation of echocardiography reports using this ten-step framework ensures comprehensive assessment while avoiding common pitfalls. For internists, understanding not just what values are abnormal but what they mean in context transforms the echo report from a list of numbers into a powerful clinical tool. Regular practice with this structured approach builds pattern recognition skills essential for expert-level interpretation. As echocardiography technology advances, the fundamental principle remains: combine systematic analysis with clinical judgment to optimize patient care.
References
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Disclosure: The author has no conflicts of interest to declare.
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