Left Sided Chamber Quantifications

• Purpose: LV size determines whether the ventricle is dilated; it can be assessed by linear or volume measurements.
• Linear technique: 2D or M-mode; 2D is recommended because it avoids oblique M-mode measurements; 2D-guided/anatomical M-mode also avoids oblique cuts.
• Edge conventions:
  • Solid structures: outer edge-to-outer edge.
  • Cavities: inner edge-to-inner edge.
  • Exceptions: aorta at all levels and left atrium in parasternal long axis use leading edge-to-leading edge because reference values were measured that way.
• Location/timing: Parasternal long-axis view at mitral leaflet tips, perpendicular to the LV long axis; end-diastole = largest LV cavity; end-systole = smallest cavity; exclude mitral valve chords.
• Sigmoid septum: In elderly patients, measure after the septal bulge, not at the bulge.
• Key measurements:
  • IVSd = interventricular septum at end-diastole
  • LVIDd = LV internal dimension at end-diastole
  • LVPWd = LV posterior wall at end-diastole
  • LVIDs = LV internal dimension at end-systole
• Clinical pearls: LVIDd determines LV size and should be indexed to BSA; LVIDs is important for timing intervention in left-sided valvular regurgitation.

• Historical linear volume calculations are no longer recommended because they assume a fixed LV geometric shape, which is inaccurate in many cardiac diseases.
• 2D methods:
  • Area-length (A-L) method: Assumes a bullet-shaped LV; uses mid-cavity area from parasternal short axis and length from apical 4-chamber, measured from mitral annular line to apex. It is not optimal because it assumes fixed geometry.
  • Method of discs / modified Simpson’s method: Recommended 2D method because it does not assume a fixed geometric shape.
• Modified Simpson’s technique:
  • Trace LV cavity in apical 4-chamber and apical 2-chamber views.
  • Avoid foreshortening.
  • Trace at the compacted myocardium–LV cavity interface, excluding trabeculations and papillary muscles.
  • Measure at end-diastole (largest cavity) and end-systole (smallest cavity).
  • Software divides LV into discs; apical 4-chamber gives D1 and apical 2-chamber gives D2; disc volumes are summed.
  • Obtain biplane LVEDV and biplane LVESV.
• Indexing: Index LVEDV to BSA.
• Ultrasound enhancing agents: Contrast use results in slightly larger LV volumes, so use cutoff values with caution.

• 3D LV volume advantages: Less relevant foreshortening, more reproducible, less operator-dependent, semi-automated.
• 3D acquisition: Optimize spatial and temporal resolution; adjust depth and set volume to include entire LV only; multi-beat acquisition usually necessary; good 2D image is prerequisite; poor 3D quality should be discarded, or UEA may be used; UEA volumes reported with caution.
• 3D upper normal limits:

• LV hypertrophy = increase in LV myocardial mass.
• Methods: linear, 2D, and 3D; all are performed at end-diastole when the LV cavity is largest.
• Linear method:
  • Use M-mode, preferably 2D-guided M-mode, or direct 2D linear measurement.
  • Well validated, extensively studied, easy and quick.
  • Cube/Devereux formula:
    LV mass (grams) = 0.8 × 1.04 × [(IVSd + LVIDd + LVPWd) × LVIDd] + 0.6 g
• 2D method:
  • Uses the A-L method similar to volume measurement.
  • Myocardial volume = LV epicardial volume − LV cavity volume, then multiplied by myocardial density 1.05.
  • LV mass = 1.05 { A₁(L + t) − [A₂L] }
    • A₁ = area of mid-LV outer border
    • A₂ = area of mid-LV cavity
    • t = LV apical thickness
  • Advantage: accommodates LV shape.
• 3D method: Software automatically traces endocardium and epicardium with manual adjustment; normal 3D LV mass reference is not yet endorsed.
• Index LV mass to BSA.

• Relative wall thickness (RWT):
  RWT = 2 × LVPWdLVIDd
• Hypertrophy classification:
  • Increased mass + RWT > 0.42 → concentric hypertrophy
  • Increased mass + RWT ≤ 0.42 → eccentric hypertrophy
  • Normal mass + RWT > 0.42 → concentric remodeling (pre-hypertrophy/earlier stage)

• Indirect clues:
  • Aortic valve M-mode: Normal box shape indicates good stroke volume; reduced stroke volume causes gradual closure in late systole → bullet shape.
  • Mitral valve M-mode points in temporal order:
    1. D = leaflet opening
    2. E = peak early-filling opening
    3. F = partial closure at mid-diastole/diastasis
    4. A = peak opening from atrial contraction
    5. C = leaflet closure
  • B-bump: Abnormal; occurs after A and before C; partial leaflet opening due to increased left atrial pressure.
  • EPSS = E-point to septal separation: Correlates with trans-mitral flow and, in the absence of significant mitral regurgitation, LV stroke volume.
    • Normal EPSS ≤ 6 mm.
    • Larger EPSS indicates decreased LV stroke volume.
• Fractional shortening (FS):
  FS(%) = LVIDd − LVIDsLVIDd × 100
  • Normal range: 25–45%
  • Limitations: measures only the basal segment; unreliable with regional wall motion abnormalities, CAD, or conduction abnormalities; not recommended as the sole measurement, should be replaced by EF.
• Ejection fraction (EF):
  EF(%) = LVEDV − LVESVLVEDV × 100
  • Volumes by 2D (A-L or MOD) or 3D.
  • ASE recommends 3D for EF because it is more reproducible; otherwise use MOD.
  • EF is a strong predictor of clinical outcome and correlates well with LV systolic function.
  • Pearl: Normal EF does not always mean normal systolic function; regional wall motion abnormality with compensatory hypercontractile segments can produce normal EF.
  • EF normal reference is the same regardless of method.
  • Increased EF above normal → report as hypercontractile/hyperdynamic LV; touching/kissing LV walls may be reported as EF > 70% instead of exact value.

• These techniques are not routinely used and cannot be the sole determinant of LV systolic function.
• Myocardial performance index (MPI / Tei index):
  • Ratio of isovolumic time to ejection time.
  • Preferred method: align PW Doppler between LVOT and mitral valve in apical 5-chamber to obtain both flows in one beat and avoid beat-to-beat variability.
  • MCOT = mitral closure-to-opening time, measured from end of mitral inflow to beginning of next beat’s mitral inflow.
  • Alternatively, MCOT = IVCT + ET + IVRT.
  • Isovolumic time = IVCT + IVRT or MCOT − ET.
  • MPI = Isovolumic timeET
  • Reflects systolic and diastolic myocardial performance; load-dependent.
  • Normal MPI ≤ 0.40; higher value = worse ventricular function.
• dP/dt:
  • Index of LV contractility; measures rate of pressure rise during isovolumic contraction at pressures below aortic pressure.
  • Measured from the mitral regurgitation signal at high sweep speed.
  • Measure time for MR velocity to increase from 1 m/s to 3 m/s.
  • By Bernoulli, this equals pressure rise from 4 mmHg to 36 mmHg, i.e., 32 mmHg.
  • dP/dt = 32t
  • Relatively load-independent because it occurs during isovolumic contraction.
  • Normal dP/dt > 1200 mmHg/s.

• Segmentation models: 16-, 17-, and 18-segment models; they differ in apical segments.
• Basic levels: Basal, mid, and apical.
• Segment numbering: Starts at the anterior segment at the junction of the interventricular septum and RV free wall as segment 1, then proceeds counterclockwise.
• Basal and mid levels: Anterior, anteroseptal, inferoseptal, inferior, inferolateral, anterolateral.
• Apical level:
  • 16-segment model: anterior, septal, inferior, lateral
  • 17-segment model: adds apical cap (segment 17)
  • 18-segment model: divides apex into six segments like basal/mid levels
• Model recommendation: 17-segment model is recommended and widely used; adopted by CMR and SPECT.
  • 16-segment ignores apical cap; 18-segment over-represents the apex.

• ASE 2015 wall motion scoring:
  • 1 = Normal/hyperkinetic: Normal wall thickening
  • 2 = Hypokinetic/tardokinetic: Reduced thickening (hypokinesis) or delayed thickening without conduction abnormality (tardokinesis)
  • 3 = Akinetic: Absent/negligible thickening
  • 4 = Dyskinetic/aneurysmal: Systolic outward bulge (dyskinetic) or systolic and diastolic outward bulge (aneurysmal)
• Wall motion score index (WMSI):
  WMSI = sum of segment scoresnumber of segments
  • WMSI = 1 is normal; higher WMSI = more extensive abnormality.
• Key point: Grade wall thickening, not wall motion, because an abnormal segment may still move due to adjacent segments and translational cardiac motion.

• Left bundle branch block (LBBB):
  • Septum is activated by the intact right bundle branch, which also activates the RV free wall; LV free wall activation is delayed by slow cell-to-cell conduction.
  • M-mode sequence:
    1. Septum thickens and moves toward the LV.
    2. RV free wall contracts unopposed by the delayed LV → septum flattens/stretches → rightward septal motion.
    3. The leftward-then-rightward movement is called septal flash.
    4. Late LV free wall activation/contraction brings the septum back toward the LV.
  • RV paced rhythm may produce similar mechanics.
  • RV apical pacing activates the LV apex first and may create the illusion of apical/septal motion abnormality.
  • Pearl: Thickening is preserved in conduction-related motion abnormalities, excluding myocardial disease.
• RV volume overload:
  • Seen in severe right-sided valvular regurgitation or left-to-right shunt.
  • RV pushes septum toward LV during diastole, mostly end-diastole → D-shaped LV in short axis; LV contour is normal/circular at end-systole.
• RV pressure overload:
  • RV pressure pushes septum toward LV during systole, mainly end-systole → flat septum and D-shaped LV.
  • RV pressure overload can also cause RV diastolic dysfunction and elevated RV end-diastolic pressure → D-shape at end-diastole as well.
  • If both RV volume and pressure overload are present → D-shape at end-systole and end-diastole.
• Paradoxical septal motion post cardiac surgery:
  • Septum moves toward the RV instead of the LV during systole.
  • Most accepted mechanism: pericardial incision releases anterior pericardial restraint → anterior motion of entire heart during systole is perceived as paradoxical septal motion.
  • Usually disappears gradually with time; may take years as cardiothoracic adhesions develop.
  • Septal thickening is preserved.
• Septal bounce: See constrictive pericarditis (chapter 16).
• Pseudodyskinesis:
  • Inferior wall moves inward during diastole (diastolic flattening) and outward during systole (systolic rounding).
  • Caused by extracardiac compression.
  • Inferior wall thickening is preserved.

• Strain/deformation: Percentage change in myocardial length.
  Strain(%) = L₁ − L₀L₀ × 100
  • L₁ = final length, L₀ = baseline length.
  • Shortening gives negative strain; lengthening gives positive strain; strain is unitless.
• Strain rate: Rate of deformation, expressed as 1/sec.
• Myocardial fiber orientation:
  • From apex: subepicardial fibers = left-handed helix; mid-layer = circumferential; subendocardial = right-handed helix.
  • Produces longitudinal, radial, circumferential contraction and twisting → wringing motion.
• Tissue Doppler method:
  • Largely replaced by speckle tracking.
  • Limitations: angle dependency (mainly longitudinal motion), poor signal-to-noise ratio, requires high frame rate ≈ 100 fps.
  • Measures velocity at two adjacent areas separated by L₀ usually 10–12 mm within the region of interest.
  • Velocity gradient = V₁ − V₂.
  • Displacement = ∫(V₁ − V₂) dt
  • Strain = displacementL₀
  • Strain rate = V₁ − V₂L₀
  • Strain = ∫ SR dt
  • If V₂ myocardium is akinetic, V₂ = V₁ because of tethering → gradient/displacement/SR/strain = 0; therefore tissue velocity alone is not useful.
  • Normal longitudinal SR wave: negative component during systole and two positive components during diastole, mirroring tissue Doppler velocities.
• Speckle tracking:
  • Grayscale speckles are unique ultrasound scatter patterns/fingerprints traced frame-by-frame.
  • Strain is measured directly; strain rate is derived from strain.
  • Not angle dependent; can calculate longitudinal, radial, circumferential strain, twist, and torsion; better noise-to-signal ratio.
  • Average strain is averaged from all 17 segments.
  • Normal averaged peak systolic longitudinal strain < −18% (more negative, e.g., −19%, −20%); normal longitudinal strain is negative, with slight vendor differences.
• Strain presentations: Table format, 17-segment bull’s eye, waveform, curved M-mode.
• Radial/circumferential strain: Obtained from short-axis view; normal radial strain is positive because radial wall thickness/length increases during systole.
• Twist and torsion:
  • From apex, cardiac base rotates clockwise (negative) and apex rotates counterclockwise (positive) during systole.
  • Twist = Apical rotation − Basal rotation
  • Torsion = Twist / Distance between apical and basal segments
  • Tissue Doppler measures them indirectly; speckle tracking measures directly; not routinely used in daily practice.

• Timing: LA size should be measured at end of LV systole, when LA is largest.
• Dedicated LA acquisition recommended because LA and LV longitudinal axes often lie in different planes; avoids foreshortening.
• Linear measurement:
  • Anteroposterior dimension in parasternal long-axis view.
  • M-mode or preferably 2D.
  • Use leading edge-to-leading edge perpendicular to LA long axis at the level of the aortic sinuses.
  • Not recommended as the exclusive LA size measure because it can be normal while LA is dilated in other planes.

• LA volume measurement:
  • Recommended approach; stronger association with outcomes than linear measurement.
  • Biplane method of discs is preferred; alternatively use biplane area-length method.
  • Area-length formula:
    Volume = 83π × A₁ × A₂L
    • A₁ = LA area in apical 4-chamber
    • A₂ = LA area in apical 2-chamber
    • L = shortest long axis from apical 2- and 4-chamber views
  • Tracing starts and ends at mitral annulus; exclude appendage and pulmonary veins.
  • Index LA volume to BSA.

• LA function:
  • Reservoir: During ventricular systole, LA receives/stores pulmonary venous blood.
  • Conduit: In early diastole after mitral valve opening, LA passes stored and pulmonary venous blood to LV.
  • Pump/boost: In late diastole, LA contracts and contributes 15–30% of entire LV filling.
• Mitral inflow spectral Doppler:
  • E wave: early diastole → reflects conduit function.
  • A wave: end-diastole → reflects pump function.
  • In atrial fibrillation, A wave is absent.
  • Mitral inflow does not correlate with LA reservoir function.
• Pulmonary vein flow spectral Doppler:
  • Three waves: S, D, Ar.
  • S wave has two components:
    • S₁: atrial relaxation draws blood from pulmonary veins
    • S₂: ventricular contraction and mitral annular apical descent draws blood from pulmonary veins
    • S₁ and S₂ usually fused on TTE, often distinct on TEE.
  • D wave: ventricular diastole when mitral valve opens; relaxing ventricle receives/sucks blood from pulmonary veins.
  • Ar wave: atrial contraction sends a little blood back into pulmonary veins.
  • S wave = reservoir function, D wave = conduit function, Ar wave = pump function.
  • In atrial fibrillation: absent effective atrial contraction/relaxation → absent S₁ component → blunted S wave; Ar wave absent.
• LA appendage flow Doppler:
  • TEE after ECG P-wave onset; reflects appendage contractile function.
  • Normal emptying velocity ≥ 50 cm/sec.
  • Velocity < 20 cm/sec is associated with LA appendage thrombus formation.
• LA strain:
  • By tissue Doppler or preferably speckle tracking; not routine; no society-endorsed reference range.
  • Most software does not support direct LA strain, so LV strain is used; baseline usually at end of QRS (ventricular end-diastole).
  • With LV end-diastole baseline:
    • Peak positive longitudinal strain (eS) = reservoir function
    • Early diastolic strain (eE) = conduit function
    • Late diastolic strain (eA) = pump function
  • With atrial cycle baseline at onset of P wave:
    • First negative peak strain (eneg) = LA pump function
    • Positive peak strain (epos) = LA conduit function
    • Total (etotal) = reservoir function

• Aortic root definition: Extends from basal attachment of aortic valve leaflets to their distal attachment at the tubular aorta, i.e., the sinotubular (ST) junction.
• Aortic root measurement:
  • Left parasternal long-axis view with adjustments to obtain the largest diameter.
  • Maximal diameter of the sinuses of Valsalva measured at end-diastole.
  • Use leading edge-to-leading edge convention, perpendicular to the long axis of the aortic root.
• Ascending aorta measurement:
  • Frequently requires moving the probe closer to the sternum and/or tilting medially.
  • Measured similarly to the aortic root.
• Indexing: Aorta measurements should be indexed to BSA.