Free RDCS Pediatric Echocardiography (PE) Exam Flashcards

In usual abdominal situs, the descending aorta is left of the spine and the IVC is anterior and rightward; situs inversus reverses that arrangement. Juxtaposed aorta/IVC or an interrupted IVC with azygos continuation can suggest heterotaxy and should trigger a systematic venous and segmental assessment. Right or left atrial isomerism concerns atrial appendage morphology; asplenia, polysplenia and venous patterns are associated findings, not interchangeable definitions or reliable proof of every intracardiac connection.

Use several features together: a moderator band, coarse apical trabeculation, septal chordal attachments and the more apical attachment of the tricuspid valve support RV morphology. A morphologic LV usually has finer trabeculation and a mitral valve without septal chordal attachments. Congenital abnormalities, common AV valves or straddling valves can complicate the assessment. D-loop and L-loop describe ventricular topology; do not turn the usual right-sided or left-sided RV arrangement into an infallible body-position rule. Establish AV and ventriculoarterial connections separately.

Trace the aorta to the morphologic LV and the pulmonary artery to the morphologic RV in multiple views. Normally the great arteries cross, and the pulmonary trunk branches into the pulmonary arteries while the aorta continues into the arch. Crossing supports the normal relationship but a single apparent angle cannot establish concordance. Parallel great arteries raise concern for transposition or another abnormal connection and require direct tracing; no universal 90-degree angle is a diagnostic criterion.

The ductus venosus carries umbilical venous blood past much of the liver to the IVC; after loss of umbilical flow it closes and leaves the ligamentum venosum. The foramen ovale permits fetal right-to-left atrial flow; rising LA pressure after birth presses its flap closed, although anatomical fusion is variable and a PFO may persist. The fossa ovalis marks the region. The ductus arteriosus connects PA to descending aorta; increased oxygen tension and falling prostaglandin levels promote constriction after birth, with the ligamentum arteriosum as its later remnant. Functional and anatomical closure occur on different timelines.

Demonstrate each coronary ostium and its proximal course using optimized parasternal short-axis sweeps plus color Doppler. Normally the RCA arises from the right aortic sinus and the left main from the left sinus before dividing into LAD and circumflex branches. Clock-face positions vary with orientation, transducer angulation and congenital anatomy, so they are navigation aids rather than proof of origin. Coronary dominance refers to the vessel supplying the posterior descending coronary artery; it does not mean the largest visible coronary.

Follow the arch relative to the airway and define every branch rather than naming sidedness from one vessel alone. In the usual left arch, the first brachiocephalic branch travels rightward and divides into right carotid and subclavian arteries. That useful pattern is not universal in abnormal branching. A common brachiocephalic/left carotid origin is often called a bovine arch variant. An aberrant right subclavian may arise distally and pass behind the esophagus; evaluate the complete arch, ductal anatomy and potential vascular ring.

A persistent left SVC commonly drains through the coronary sinus into the RA and can enlarge the coronary sinus. Dilation is a clue, not a diagnosis: inspect systemic venous connections and consider other causes. When clinically appropriate under the laboratory protocol, left-arm agitated saline may opacify the coronary sinus before the RA. Drainage to the LA, including through an unroofed coronary sinus, changes the shunt implications; define the actual drainage instead of assuming every left SVC is harmless.

Outflow tract development involves several interacting tissues, including cardiac neural crest cells, and abnormal development can contribute to conotruncal malformations such as TOF or truncus arteriosus. Endocardial cushion and AV junction development are important to AV septation and AV valve formation. These associations help organize morphology, but there is no single failed 180-degree fusion event that fully explains every listed defect. Describe the actual septal, valvar and outflow connections rather than assigning a uniform embryologic cause.

Using body-surface-area-indexed internal lumen diameters of the LMCA, LAD, and RCA: Normal is Z < 2.0; Dilation only is Z 2.0 to < 2.5; Small aneurysm is Z ≥ 2.5 to < 5.0; Medium aneurysm is Z ≥ 5.0 to < 10.0 with an absolute internal diameter < 8 mm; Giant aneurysm is Z ≥ 10.0 or an absolute internal diameter ≥ 8 mm. Acute Kawasaki echo studies also evaluate for perivascular brightness, pericardial effusion, mitral regurgitation, and depressed LV systolic function.

DCM typically combines ventricular dilation with reduced systolic function, sometimes with secondary AV valve regurgitation. HCM involves otherwise unexplained myocardial hypertrophy assessed against appropriate pediatric reference data; hypertrophy may be asymmetric or concentric. Diastolic dysfunction may occur, while systolic anterior mitral motion, dynamic LVOT obstruction and a late-peaking Doppler jet occur only in obstructive forms. A small hyperdynamic cavity or obstruction is not required in every HCM case. Interpret measurements with loading conditions, family history and the full phenotype.

Vegetations often attach to the upstream, lower-pressure valve surface: atrial for AV valves and ventricular for semilunar valves; abnormal jet impact sites can also be involved. Examine valve function, surrounding tissue and other complications. A negative study does not alone exclude infective endocarditis. Acute rheumatic carditis can cause mitral or aortic regurgitation through valvar inflammation and altered leaflet/chordal function. Chronic rheumatic disease may produce thickening, chordal changes and commissural fusion with diastolic doming, but not every acute episode progresses to the same chronic lesion.

Integrate TR jet velocity, septal configuration, RV size/function and shunt direction. With a suitable TR envelope, RVSP is estimated as 4v² plus RA pressure; it approximates PASP only without RV outflow or pulmonary valve obstruction. Systolic septal flattening supports RV pressure loading. Pulmonary acceleration time depends on heart rate, age and loading, so a single PAAT below 90 ms does not diagnose severe pulmonary hypertension in every child or newborn. Transitional neonatal physiology and ductal/atrial shunts require particular context.

An effusion can impair filling when intrapericardial pressure exceeds chamber pressure. Findings may include RA inward collapse during ventricular systole, RV free-wall collapse during early diastole, a plethoric IVC and exaggerated respiratory variation in AV inflow. Their sensitivity depends on filling pressures, ventilation, location of fluid and the clinical setting; pulmonary hypertension or a loculated postoperative collection can alter the usual pattern. Do not equate fluid size alone with tamponade or apply spontaneous-breathing Doppler thresholds without checking ventilation.

Assess chamber dimensions, wall thickness, global and regional systolic function, AV valve regurgitation and pericardial fluid against prior studies. Myocardial inflammation can produce dysfunction with edema and little initial dilation; other presentations occur. Longitudinal strain can identify subtle dysfunction before a fall in EF, including during cardiotoxic therapy, but depends on image quality and vendor/method consistency. No isolated strain, tissue Doppler or effusion finding proves myocarditis or transplant rejection; integrate the clinical assessment and appropriate additional tests.

A secundum ASD is in the fossa ovalis region. A primum defect is part of the AV septal defect spectrum near the AV junction. Superior or inferior sinus venosus defects occur near caval connections and may accompany anomalous pulmonary venous drainage. An unroofed coronary sinus communicates with the LA. A substantial net left-to-right shunt can enlarge the RA/RV and cause diastolic septal flattening; tiny or differently directed communications do not invariably cause that loading pattern. Define rims, venous return and shunt physiology.

Describe the defect's borders and its relationship to the valves and ventricular septum. Perimembranous defects adjoin the membranous area; muscular defects have muscular rims; inlet defects lie near the AV valve inlet; doubly committed subarterial/outlet defects lie beneath the semilunar valves. Defects with inadequate aortic cusp support can develop cusp prolapse and aortic regurgitation. Use multiple views and color Doppler; fixed clock-face positions or population percentages cannot replace direct anatomic definition.

A typical left-sided duct connects the proximal descending aorta near the left subclavian artery to the pulmonary artery near the LPA origin. A high parasternal ductal view and other sweeps define the connection. With lower pulmonary than systemic pressure, flow is usually aorta-to-PA through systole and diastole; higher pulmonary pressure can produce bidirectional or PA-to-aorta flow. Doppler color depends on direction relative to the probe and the selected map, so a red flame is not a universal diagnostic sign.

Identify the common AV junction, atrial and ventricular components, bridging leaflets, ventricular balance and outflow relationships. A common AV valve often has five leaflets, with loss of normal AV valve offset and an elongated LVOT. Rastelli classification describes superior bridging leaflet attachments: A attaches toward the septal crest, B to an anomalous RV papillary muscle and C bridges freely without septal attachment. It does not substitute for describing the patient's actual valve tissue, chordae, regurgitation and surgical anatomy.

TOF combines an anterior-malalignment VSD, overriding aorta, RV outflow obstruction and RV hypertrophy. Outlet septal deviation and surrounding muscle anatomy contribute to obstruction, which can be subvalvar, valvar or more distal. Assess the degree of aortic override directly rather than treating one percentage as the entire definition. Trace coronary origins and any large branch crossing the RVOT, especially an LAD arising from the RCA, because its course affects a planned RVOT incision. Also assess pulmonary arteries and arch anatomy.

D-TGA usually has AV concordance with ventriculoarterial discordance: the aorta arises from the morphologic RV and PA from the LV, creating parallel circulations dependent on adequate mixing. Congenitally corrected TGA has both AV and ventriculoarterial discordance, giving a series circulation but a morphologic RV and tricuspid valve in the systemic circuit. Typical segmental patterns are {S,D,D} and {S,L,L}, respectively, but situs and vessel position can vary. Diagnose the actual connections, not the letter pattern or aorta position alone.

Assess for VSD, obstruction of the pulmonary outflow from the morphologic LV, and abnormalities of the systemic tricuspid valve, including Ebstein-like displacement and regurgitation. The systemic morphologic RV may develop dysfunction, and the abnormal conduction system increases the risk of AV block. These are important associations rather than a mandatory triad in every patient. Follow chamber morphology, valve function, gradients and rhythm context without using unsourced prevalence percentages or a fixed annual event risk as an individual prediction.

Define the arch, branch pattern and isthmus in suprasternal and other suitable views, measuring dimensions with appropriate Z scores. A discrete juxtaductal shelf or diffuse arch hypoplasia may be present. Doppler can show accelerated systolic flow, persistent forward diastolic flow and a damped abdominal aortic waveform. Gradients depend on flow, ventricular function, a patent ductus and collateral circulation; a low velocity does not exclude critical narrowing. Look for bicuspid aortic valve, other left-sided obstruction and associated septal defects.

Define mitral and aortic valve patency, LV size/function, ascending aorta and arch, atrial communication, pulmonary venous flow and the PDA. The spectrum includes different combinations of atresia and stenosis. In severe aortic atresia, systemic and coronary perfusion depend on ductal flow with retrograde arch/ascending aortic flow; not every HLHS variant has an identical flow pattern. Restrictive egress from the LA is hazardous, so assess the atrial communication and pulmonary venous Doppler rather than assuming unrestricted mixing.

TAPVR has no normal pulmonary venous connection to the LA. Drainage is classified as supracardiac, cardiac, infracardiac or mixed; an atrial communication permits blood to reach the left heart. Infracardiac drainage often descends through the diaphragm to portal, hepatic or systemic venous channels and has a high obstruction risk. Trace every vein, the confluence and the entire drainage channel, integrating narrowing and Doppler phasicity rather than one universal velocity cutoff. PAPVR affects some veins; Scimitar syndrome typically includes anomalous right pulmonary venous drainage toward the IVC and right lung abnormalities.

In an apical four-chamber view, septal tricuspid leaflet displacement indexed to BSA at or above 8 mm/m² relative to the mitral insertion supports Ebstein anomaly. It is not the entire diagnosis. Describe failed leaflet delamination, tethering, the atrialized RV, functional RV, tricuspid regurgitation and pulmonary outflow. An atrial communication may permit right-to-left shunting, and accessory pathways may coexist. The degree of displacement alone does not predict every patient's physiology.

A common arterial trunk supplies systemic, pulmonary and coronary circulations through one truncal valve, usually with a large outlet VSD. Define the pulmonary artery origins, truncal valve morphology and function, coronary anatomy and arch. In Collett–Edwards descriptions, type I has a short main pulmonary trunk, while II and III have separately arising branch pulmonary arteries with different spacing/origins. The lesion is associated with 22q11.2 deletion and arch abnormalities, but neither a fixed percentage nor a right arch is required for diagnosis.

ALCAPA means the left coronary originates from the pulmonary artery; after pulmonary pressure falls, findings can include retrograde coronary flow toward the PA, LV dysfunction, mitral regurgitation and collateral flow. AAOCA concerns an abnormal aortic origin, often from the opposite sinus. Define its ostium and proximal course, including an intramural segment or an interarterial course. Not every coronary variant has the same risk, and normal ventricular function does not exclude important coronary anatomy; incomplete visualization should not be labeled normal.

A modified BTT shunt connects a systemic artery, commonly subclavian or brachiocephalic, to a pulmonary artery. It commonly has forward flow in both systole and diastole and may produce systemic diastolic runoff. A Sano conduit connects the RV to the PA and commonly has systolic forward flow with diastolic regurgitation when nonvalved. Assess the actual conduit design, patency, narrowing and flow; neither an expected waveform nor reduced runoff guarantees adequate pulmonary or coronary perfusion.

Reconstruction establishes a systemic outflow through a neoaorta/arch, unobstructed pulmonary venous egress through the atrial communication, and a controlled source of pulmonary blood flow through a systemic-to-PA shunt or RV-to-PA conduit. Echo checks the reconstructed arch, atrial communication, shunt/conduit and branch PAs, systemic ventricular function, AV valve regurgitation and neoaortic valve function. This is palliation, not restoration of normal biventricular anatomy; review the operative report because techniques vary.

The SVC is connected to the pulmonary arterial circulation so upper-body venous return reaches both lungs without a subpulmonary ventricular pump. Lower-body venous return still reaches the heart before later completion. Assess the anastomosis and branch PAs for unobstructed, low-velocity flow with appropriate respiratory/cardiac variation, along with venous collateral pathways and ventricular/AV valve function. Age at surgery, flow patterns and velocities vary with anatomy and loading; a single fixed velocity threshold does not establish obstruction or elevated PA pressure.

Fontan completion directs systemic venous return to the pulmonary arteries through a total cavopulmonary pathway, commonly using a lateral tunnel or extracardiac conduit. A fenestration connects that pathway to the pulmonary venous atrium, allowing right-to-left decompression at the cost of desaturation. Doppler can estimate the pressure difference across the actual communication under appropriate assumptions; use the mean tracing when discussing a mean gradient. Do not equate a single peak 4v² value with a universal transpulmonary gradient, pulmonary resistance or a normal range for every Fontan.

The Jatene ASO transects both great arteries above their sinuses, translocates them to their anatomic ventricles, excises the coronary artery ostia as buttons and reimplants them into the neoaortic root (former pulmonary root), and performs the LeCompte maneuver—bringing the pulmonary artery bifurcation anterior to the ascending neoaorta so the RPA and LPA drape astride it. The three classic late complications on echo are: (1) supravalvular pulmonary stenosis and branch PA stenosis (stretched across the anterior neoaorta, best seen in high parasternal/suprasternal views), (2) neoaortic root dilation and neoaortic valve regurgitation, and (3) coronary ostial stenosis or kinking causing LV wall-motion abnormalities.

Atrial baffles redirect systemic venous return toward the mitral valve and morphologic LV/pulmonary circuit, and pulmonary venous return toward the tricuspid valve and morphologic RV/systemic circuit. Mustard uses baffle material; Senning uses atrial tissue. The great artery connections remain transposed. Surveillance addresses systemic RV function, systemic tricuspid regurgitation, systemic and pulmonary venous pathway obstruction and baffle leaks. Correlate anatomy, flow and loading rather than diagnosing every baffle obstruction from one velocity cutoff.

For suitable anatomy such as TGA with VSD and pulmonary outflow obstruction, an intraventricular tunnel routes LV output through the VSD to the aorta, while an RV-to-PA conduit provides pulmonary outflow. The operation is selected according to detailed anatomy; it is not the only possible repair for every TGA/VSD/PS patient. Postoperative echo assesses the LV-to-aorta tunnel, residual shunts, conduit stenosis/regurgitation and ventricular function, using the operative report to establish the actual reconstruction.

The native pulmonary valve/root is moved into the aortic position as an autograft, and the RV-to-PA pathway receives a homograft or other conduit. The living autograft has growth potential and usually avoids the lifelong anticoagulation required solely for a mechanical valve, but it is not free of complications. Follow the autograft/root for dilation or regurgitation and the RV-to-PA conduit for obstruction or regurgitation; assess ventricular responses as well. Other patient-specific indications for anticoagulation remain possible.

A transannular patch can produce important pulmonary regurgitation with progressive RV volume loading; residual RVOT or branch PA obstruction may coexist. Integrate color and spectral Doppler, forward/reverse PA flow, RV size/function and the repaired VSD. A short, rapidly decelerating PR envelope can support severe regurgitation but also depends on PA/RV pressures and restrictive RV physiology. Do not use one pressure half-time or a claimed holodiastolic pattern as an infallible severity rule for every child.

With velocities in m/s, simplified modified Bernoulli gives ΔP in mmHg as 4v² when proximal velocity is negligible and the assumptions are appropriate. If proximal kinetic energy matters, consider 4(v₂²−v₁²) rather than ignoring it. Serial or long-segment obstruction, poor alignment, pressure recovery and viscous losses complicate interpretation; subtracting one velocity does not automatically solve a multilevel lesion. The peak estimate is maximum instantaneous pressure difference, not catheter peak-to-peak pressure or a mean gradient.

Stroke volume is cross-sectional area × VTI; for a circular section, area = πd²/4. A flow ratio uses measurements at sites representing pulmonary and systemic flow, with heart rate considered if recordings differ. For an isolated intracardiac left-to-right shunt without significant semilunar regurgitation, RVOT flow can exceed LVOT flow. A PDA enters the PA distal to the pulmonary valve, so LVOT flow can instead exceed RVOT flow. Define the anatomy, sampling sites and other shunts/regurgitation before calling a valve-level ratio Qp:Qs or using it to judge clinical significance.

For an adequate, aligned TR envelope, RVSP ≈ 4vTR² + estimated RA pressure. For a restrictive left-to-right VSD, the LV-to-RV gradient can be subtracted from LV systolic pressure; systemic cuff SBP is a surrogate only when appropriate and without important LV outflow obstruction. For SBP 100 mmHg and vVSD 4 m/s, ΔP 64 mmHg gives RVSP≈36 mmHg. RVSP approximates PASP only without RV outflow/pulmonary valve obstruction; poor envelopes, pressure timing and RA pressure uncertainty can materially change estimates.

A Z score expresses deviation from the reference mean relative to the model's variability, usually accounting for body size; 0 is the reference mean. About −2 to +2 is a familiar reference interval under an approximately normal model, not a standalone diagnosis. Record accurate height/weight and use the correct measurement location, timing, edge convention and reference model. Different models can give different Z scores for the same measurement. Use one consistent model for serial follow-up; a 2D-derived reference should not automatically be applied to M-mode measurements.

Use the highest frequency that still provides adequate penetration for the patient's size and acoustic window, balancing spatial and temporal resolution. For small coronary or low-velocity venous flow, reduce the color scale appropriately, optimize gain and focus, and limit sector size to maintain frame rate. Increase the scale when needed to avoid misleading aliasing. Fixed age-to-frequency bands or one Nyquist value cannot be prescribed for every child, transducer and target; confirm that the setting displays the actual flow of interest.

Subcostal views help establish abdominal situs, systemic venous connections, atrial septum and cardiac connections, often with the septum more perpendicular to the beam. The suprasternal short-axis crab view can demonstrate pulmonary veins entering the LA. Each vein should be individually traced with color/Doppler rather than assuming a recognizable shape proves normal return. ASE 2024 accepts laboratory protocols beginning with subcostal or parasternal views; it does not mandate one sequence, and perpendicular imaging reduces rather than eliminates artifacts.

ASE 2024 describes aortic and pulmonary annular diameters from inner edge to inner edge at leaflet hinge points during maximal opening in early to mid-systole. Pediatric aortic diameters are measured inner-edge to inner-edge at their maximum dimension during peak flow in mid-systole, consistently with the chosen pediatric reference data. This differs from traditional adult diastolic leading-edge conventions. Do not generalize systolic timing to every vascular measurement: for example, the RVOT diameter can use end-diastole, and AV annular measurements use diastole.

SF (%) = 100 × (LVEDD−LVESD)/LVEDD using correctly timed, consistently located LV minor-axis dimensions. It samples radial shortening and should not be used as a reliable global measure when regional wall motion or noncircular geometry invalidates that dimension. Use an integrated assessment with appropriate volumetric EF methods, such as Simpson biplane, bullet area-length or feasible 3D, rather than requiring one method for all cases. Loading, image quality and reference methods matter; a single universal pediatric SF/EF cutoff is insufficient.

Combine qualitative assessment with measures suited to the anatomy: TAPSE for annular longitudinal excursion, FAC = 100 × (end-diastolic area−end-systolic area)/end-diastolic area, tissue Doppler s′, and selected strain or 3D measurements. TAPSE/FAC do not fully capture RVOT function, and measurements depend on geometry, loading and image quality. Compare with appropriate pediatric reference data and prior studies; do not apply an adult FAC threshold alone as a universal pediatric normality test.

MPI = (isovolumic contraction time + isovolumic relaxation time)/ejection time. With compatible interval measurements it can also be written (a−b)/b, where a spans AV closure to opening and b is ejection time. It combines systolic/diastolic timing without a chamber-shape formula, but depends on loading, heart rate and measurement method. ASE 2024 notes high variability and limited usefulness in the normal RV, with potential value in selected abnormal loading states. Do not diagnose dysfunction or select MPI alone from a universal normal range.

Without angle correction, the measured component is v×cosθ; a gradient derived from 4v² changes with cos²θ. At 20°, velocity is about 6% lower and the squared gradient about 12% lower; at 60°, the respective underestimates are 50% and 75%. Seek the best parallel alignment from multiple windows. PW aliasing occurs beyond the Nyquist limit (PRF/2): appropriate scale/PRF, depth or frequency changes may help, or CW may be needed for high velocities. Baseline shift can change the display but does not increase the underlying Nyquist sampling limit.

The thin atrial septum may look deficient when parallel to the apical beam. Use subcostal or other perpendicular views, multiple planes and appropriate color/Doppler to establish an actual communication, its rims and physiology. Assess pulmonary venous connections and right-heart loading where relevant. A T-shaped rim artifact, a single color jet or a fixed velocity-scale setting alone is not proof of a defect, and a small or differently directed shunt need not produce the usual RA/RV dilation.

Count from RA opacification. ASE 2024 describes left-heart contrast within 3–6 cycles as suggesting interatrial shunting, and later than 6 cycles as raising suspicion of intrapulmonary shunting. These are clues, not an infallible timing-only diagnosis: follow the entry route and consider pressure, maneuvers and circulation. Left-arm injection can help define a left SVC through coronary-sinus opacification; an unroofed sinus can opacify RA/LA. Site and anatomy matter particularly after cavopulmonary surgery. Apply the laboratory's clinically appropriate contrast protocol.

Peak CW Doppler velocity estimates the largest instantaneous pressure difference using the appropriate velocity equation. Catheter peak-to-peak gradient compares peak ventricular and peak arterial systolic pressures that generally occur at different times. Pressure recovery, physiologic state and measurement location can add to disagreement, especially in small children. Doppler commonly exceeds peak-to-peak measurements, but there is no universal fixed difference or guarantee for every recording. Compare like measurements and integrate morphology, flow and ventricular function.