Free ARDMS AE Exam Flashcards

The aorto-mitral curtain is the fibrous continuity between the anterior mitral leaflet and the adjacent aortic root, especially the left and noncoronary cusps. It links LV inflow and outflow anatomy.

It drains into the posteroinferior right atrium near the IVC and septal tricuspid annulus. A dilated coronary sinus should prompt correlation for elevated right-sided pressure or abnormal venous drainage.

Coarse trabeculations, a moderator band, and a tricuspid valve inserted more apically than the mitral valve favor the RV. Use several features together because one view may be misleading.

The right and left coronary arteries normally arise from their corresponding aortic sinuses. The third is termed the noncoronary sinus because it normally has no coronary ostium.

During isovolumic contraction and isovolumic relaxation. Ventricular pressure changes rapidly in both intervals, but ventricular volume does not change because no valve is open.

Inspiration increases systemic venous return, so right-sided inflow velocities usually rise. Left-sided inflow often falls modestly because of changing pulmonary venous return and ventricular interaction.

Wall thickening and contractility increase, while the end-systolic cavity becomes smaller. Failure to augment or a new regional abnormality requires physician interpretation in the full stress-test context.

E reflects early passive LV filling; A reflects filling from atrial contraction. Their relative sizes vary with age, rhythm, relaxation, compliance, and loading, so the E/A ratio is not interpreted alone.

A late-peaking, dagger-shaped systolic CW envelope, often with systolic anterior mitral motion, supports dynamic obstruction. Reduced preload during Valsalva can intensify it; record the physiologic state with the gradient.

Relative apical sparing of longitudinal strain can support an infiltrative pattern when paired with increased wall thickness and other findings. It is not specific enough to diagnose amyloidosis by itself.

The LV is enlarged and more spherical with diffuse systolic dysfunction. Annular enlargement and papillary displacement may produce secondary mitral regurgitation even when the leaflets are structurally normal.

Respiration-related septal shift, marked respiratory Doppler variation, and preserved or increased medial e' favor constrictive physiology. Restriction more often lowers myocardial e'; diagnosis requires an integrated study.

Tamponade is hemodynamic, not merely an anatomic fluid measurement. Chamber collapse, IVC plethora, respiratory flow changes, accumulation rate, blood pressure, and the patient's clinical condition must be integrated.

The LV may still be normal in size because remodeling has not occurred. Rapid pressure equalization, premature mitral closure, and clinical instability can be important; pressure half-time remains load- and compliance-dependent.

A wall-hugging jet loses momentum along the atrial wall and may occupy little color area. Integrate valve anatomy, vena contracta, quantitative Doppler when feasible, pulmonary venous flow, and chamber response.

First verify Doppler alignment from multiple windows, LVOT diameter and sample placement, rhythm, blood pressure, and flow. Then integrate velocity, mean gradient, calculated area, and stroke-volume index rather than forcing one cutoff.

With increased flow, a fixed severely restricted valve shows little area increase while velocity and gradient rise. A valve that opens substantially more suggests pseudo-severe stenosis; the supervising physician integrates the complete response.

Commissural fusion, diastolic doming, leaflet-tip thickening, and subvalvular shortening favor rheumatic disease. Direct planimetry is useful when the orifice is well seen; pressure half-time has important physiologic limitations.

LV or atrial remodeling alters annular geometry and leaflet coaptation despite structurally normal leaflets. Ventricular disease often causes apical tethering; severity can change with loading and should be assessed integratively.

Prominent systolic flow reversal in the hepatic veins supports severe TR when rhythm and sampling are appropriate. Combine it with valve anatomy, vena contracta, CW density and shape, and right-heart remodeling.

A new irregular thickening or echo-free cavity beside an infected valve, especially with dehiscence or fistulous flow, is concerning. Document and communicate urgently; endocarditis diagnosis also depends on clinical and microbiologic evidence.

A mobile stalk at the fossa ovalis favors myxoma; an appendage mass in atrial fibrillation or marked stasis favors thrombus. Attachment, mobility, spontaneous contrast, and multiple views matter more than echogenicity alone.

Septal rupture produces turbulent left-to-right flow through a new ventricular defect. Papillary muscle rupture produces a flail mitral leaflet with acute severe MR, sometimes with a mobile muscle head. Both require immediate escalation.

Flattening greatest in systole favors RV pressure overload; flattening greatest in diastole favors RV volume overload. The pattern is not specific for pulmonary embolism and must be correlated with the full right-heart study.

A true flap has consistent independent motion, separates two lumens, and persists in orthogonal views, sometimes with different Doppler flow. Reverberation can mimic a flap; suspected ascending dissection is a critical finding for urgent communication.

A high gradient can reflect increased flow or patient-prosthesis mismatch as well as true obstruction. Compare with the baseline study and the valve's type and size, then integrate leaflet or occluder motion, flow state, Doppler contour, acceleration time, dimensionless index, effective orifice area, and change in gradient.

An ASD is a persistent tissue defect that can sustain left-to-right flow and cause RA/RV volume overload. A PFO is a flap-like potential channel and usually does not create chronic right-heart volume overload by itself.

Dysfunction extending beyond a single coronary distribution, often with a characteristic ballooning pattern, favors stress cardiomyopathy. Echo supports the pattern but does not replace clinical evaluation and coronary assessment.

Confirm and document within competence, remain attentive to the patient, and use the facility's urgent communication pathway to the responsible clinician. The sonographer communicates findings but does not independently make the final diagnosis or prescribe treatment.

An intact-skin TTE probe generally receives approved low-level disinfection. A TEE probe contacts mucous membranes and requires cleaning followed by validated high-level disinfection, storage, and traceability under manufacturer and facility instructions.

Verify identity, order, consent, fasting status under local policy, esophageal history, medications and allergies, monitoring, airway and sedation plans, and emergency readiness. Escalate contraindication concerns to the procedural clinician.

Stop the stress portion according to protocol, alert the supervising clinician, monitor the patient and ECG, and activate the facility's emergency response as directed. Do not independently choose or administer treatment outside authorized protocol.

Stop administration, maintain observation and monitoring, immediately alert the responsible clinician, and follow the site's emergency protocol. Record the event accurately; treatment decisions follow standing orders or authorized clinical direction.

EF = (EDV − ESV) / EDV × 100%. EDV is the end-diastolic volume and ESV the end-systolic volume; EF is a volume fraction and remains load-dependent.

CSA = π(d/2)², commonly written 0.785 × d². If diameter d is measured in cm, CSA is in cm². Because diameter is squared, a small diameter error produces a much larger area, stroke-volume, and continuity-equation error.

Stroke volume = outflow-tract CSA × VTI. With CSA in cm² and VTI in cm, stroke volume is in cm³, equivalent to mL. Cardiac output = stroke volume × heart rate; divide mL/min by 1,000 for L/min. Use matched sampling locations, and recognize that rhythm and diameter error affect precision.

AVA = (CSA_LVOT × VTI_LVOT) / VTI_AV. With CSA in cm² and both VTIs in cm, AVA is in cm². PW Doppler samples LVOT flow at the same anatomic level used for its area and before acceleration; CW Doppler captures the highest valid valve jet from multiple windows.

Use ΔP = 4(v₂² − v₁²) when proximal velocity is not negligible. Enter both velocities in m/s to obtain ΔP in mmHg. The shortcut ΔP = 4v₂² assumes v₁ is small; ignoring a high proximal velocity overstates the net gradient. Mean gradient still comes from averaging instantaneous gradients along the traced envelope, not 4 × mean velocity².

RVSP = 4(TR peak velocity)² + estimated RA pressure. Use TR velocity in m/s; 4v² and RA pressure are in mmHg. RVSP approximates pulmonary artery systolic pressure only when there is no significant RV outflow, pulmonic-valve, or proximal pulmonary-artery obstruction.

For native mitral stenosis, MVA (cm²) ≈ 220 / PHT (ms). The estimate can be unreliable with changing chamber compliance, significant aortic regurgitation, or soon after valvotomy; atrial fibrillation requires suitable beat selection and averaging. It is not a stand-alone result.

Flow rate = 2πr² × aliasing velocity. With r in cm and aliasing velocity in cm/s, dividing flow rate by peak regurgitant velocity in cm/s gives EROA in cm²; EROA × regurgitant VTI in cm gives regurgitant volume in mL. Constrained or nonhemispheric geometry and eccentric, multiple, or markedly time-varying jets can violate key assumptions.

Qp/Qs = (RVOT CSA × RVOT VTI) / (LVOT CSA × LVOT VTI). The ratio is dimensionless; values above 1 suggest net left-to-right shunting. Semilunar regurgitation, mismatched measurement sites, and diameter-squared error can distort the estimate.

Apical foreshortening truncates the true long axis and underestimates volumes. Acquire dedicated nonforeshortened apical four- and two-chamber views, then trace end-diastolic and end-systolic endocardial borders consistently.

PW transmitral flow is sampled at the leaflet tips; tissue Doppler e' is sampled at the septal and lateral annulus. E and e' must use the same velocity units so E/e' is dimensionless. The ratio contributes to filling-pressure assessment but must be integrated with other diastolic variables and the clinical setting.

The ultrasound beam is more nearly perpendicular to the septum, reducing false dropout. Confirm a suspected defect with orthogonal imaging and color Doppler rather than labeling dropout as pathology.

Valsalva strain reduces venous return and LV cavity size, which can provoke dynamic obstruction. Record rest, strain, and recovery, and trace a clean LVOT envelope without contaminating it with mitral regurgitation.

The Doppler shift exceeds the Nyquist limit, equal to PRF/2. Raising PRF or scale increases the Nyquist limit; shifting the baseline only reallocates the displayed range to one direction. CW Doppler measures higher velocities without this Nyquist limit but sacrifices range specificity.

Measured velocity equals true velocity × cos θ. Align as parallel as possible and use multiple windows; routine angle correction is not recommended for cardiac Doppler. Increasing angle causes underestimation, and Bernoulli-derived gradient error is magnified because velocity is squared.

Reduce depth, narrow the sector, and limit focal zones to what the target requires. These changes raise frame rate, with a tradeoff in field of view or spatial detail.

Low-MI contrast-specific imaging preserves circulating microbubbles while suppressing tissue signal. High acoustic output destroys bubbles; a deliberate brief high-MI flash is used only when a replenishment assessment is intended.