Assessment can be challenging due to shape and extensive trabeculations.

Important for critical care – CO has to equal CO of left heart and function is arguably more important given the RV’s sensitivity to fluid balance, positive pressure ventilation and many crit care pathologies.

RV – inflow and outflow regions.

Contracts longitudinally, radially (free wall towards septum) and rotation pulled by LV.

Pulmonary vasculature is a low pressure system so RV is less muscular than LV.

Ejection of SV continues into its relaxation so outflow is semi continuous.

Dilates acutely in response to increased afterload and is able to become hypertrophied in 48hrs.

RV is perfused in both systole and diastole so function is dependent on adequate MAP.

Key features of RV peristaltic movement:

  • Infundibular expansion occurs just prior to contraction.
  • Infundibular contraction occurs 20-50ms after contraction of RV free wall.
  • Longitudinal shortening contributes most to RV free wall contraction.
  • Transverse shortening (RV free wall moving towards septum) also occurs.
  • LV contributes to RV ejection by bulging into RV cavity.
  • Low pressure within pulmonary vasculature encourages blood flow to continue forwards even after RV pressure has decreased to value below that of the PA.

RV and PA must be viewed as a coupled unit – RV-PA coupling.

Compliance of pulmonary system 2ml/mmHg.

RV tolerates PA pressure changes poorly. RV can accommodate and react appropriately to changes in volume.

More on PA pressure and PVR in relevant sections.

Views:

  • PLAX
  • Parasternal RV inflow view
  • Parasternal RV outflow view
  • PSAX
  • Modified A4C
  • Subcostal

Assessment:

Should include:

  • RV dimensions – cavity size & wall thickness
  • Global systolic function
  • Regional systolic function
  • RV masses/thrombus.

Dimensions:

Visual assessment – RV should be 2/3 the size of LV. If it is the same size then dilated.

Remember moderator band may be seen in apex and trabeculations will be present.

Parasternal short axis view (AV level):

  • RVOT diameter at aortic valve level.
  • RVOT diameter at pulmonary valve.
  • Main pulmonary artery diameter.

Modified A4C:

  • Basal RV diameter.
  • Mid RV diameter.
  • RV long axis length (base to apex).

PLAX/Subcostal:

  • RV free wall thickness. Normal <5mm.
  • Chronic cor pulmonale associated with thickened RV – 10-12mm.
  • Only mild thickening occurs in acute cor pulmonale. E.g. only slight thickening of 5-6mm seen within 3 days of starting mechanical ventilation.

Eccentricity index:

RV/LV ratio:

  • 0.8-1.0 in mild dilation
  • 1.1-1.4 in moderate dilation
  • 1.5 in severe RV dilation.

In PSAX – LV should have circular cross-section.

If there is RV volume or pressure overload then the septum becomes flattened and LV becomes D shaped.

  • Predominantly volume overload is seen as LV septal flattening in end diastole. As RV pressure increased relative to LV.
  • Predominantly pressure overload seen as LV septal flattening in end-systole. As RV pressure is increased, RV ejection time is prolonged.

Eccentricity index: degree of flattening quantified. Measure of ratio of LV anteroposterior diameter to LV septolateral diameter.

EI = LVAP / LVSL

  • Normal – 1.0.
  • Mild – 1.1-1.4.
  • Moderate – 1.5-1.8.
  • Severe – > 1.8 in severe septal bowing.

RV function:

Can often be eyeballed.

Can also be affected by RWMAs – RV free wall, apex, IVS, RVOT anterior wall.

Quantitively can also be assessed by:

  • TAPSE
  • TDI – RVS’
  • Fractional area change
  • Tei index
  • Dp/dt

TAPSE:

Tricuspid annular plane systolic excursion. M-mode at lateral tricuspid annulus measuring longitudinal function.

Remember when annulus is fixed (e.g. TV ring annuloplasty) the annulus will be fixed and TAPSE/TDI cannot be used.

Normal >1.6cm.

TDI – RVS’:

Measured from the base of RV free wall. Looks similar to TDI of LV wall.

RVS’ is an additional measure of longitudinal RV function.

Lower limit of normal is 10cm/s.

Fractional area change:

In modified A4C view trace RV diastole and ssytole.

Volume isn’t calculated as crescent shape of RV is not amenable to Simpson’s disc method.

Normal >32%

FAC = (RVEDa – RVESa) / RVEDa x 100

RV stroke volume:

Same method as for LV SV – measure RVOT diameter then trace the VTI across pulmonary valve/RVOT.

Value of <12 to 15 indicates reduced RV stroke volume.

RV ejection fraction:

Simpson’s not accurate.

Need 3D echo.

Tei index (myocardial performance index):

More complex and less frequently used. Calculated as ratio between time taken for the ejection and non-ejection work of the ventricle according to:

MPI = (IVCT + IVRT)/ET

Either measured using two separate images with PW doppler across TV inflow & RV outflow or using TDI in one view at the TV annulus..

If using pulsed wave – upper limit 0.40.

If using TDI – upper limit 0.55.

RV dP/dt (change in wall pressure/time):

Same method as for MR.

If full TR envelope is seen measure time required for regurg jet to increase in velocity from 1 to 2m/s (as opposed to 1-3m/s in MR).

According to Bernoulli equation, this represents a 12mmHg increase in pressure (4mmHg to 16mmHg).

dP/dT is calculated by dividing 12mmHg by the time measured in seconds.

Remains a load dependent variable and limited normal range data for it.

RV diastolic function:

Difficult to assess.

May be an early sign of RV impairment or poor prognostic sign in those with known dysfunction.

Usually present before systolic dysfunction/dilation/hypertrophy.

Measure:

  • TV inflow pattern – PW
  • TDI at tricuspid annulus
  • RA size – upper limit of normal 18cm^2

Grading:

  • Tricuspid E/A ratio <0.8 – impaired relaxation.
  • E/A ratio 0.8-2.1 with E/e’ >6 suggests pseudonormal pattern.
  • E/A ratio >2.1 with DT <120ms suggests restrictive filling.

Late diastolic antegrade flow in PA also a sign of restrictive filling.

High pressure in late diastole causes PV to open before systole and forward flow to occur.

Cor pulmonale:

Acute or chronic.

Gradual RV thickening and increase in RH systolic and diastolic pressures which lead to 2 key features of chronic cor pulmonale:

  • RV can generate high pressure TR jets of >60mmHg which is not seen in acute cor pulmonale without prior conditioning of RV. Can occur regardless of size of TR jet which is unrelated to its pressure in this setting.
  • RVH maintains RV structure until later in cor pulmonale when thickened ventricle begins to fail and dilate. Therefore significant RV dilation should be considered a sign of acute cor pulmonale or late chronic cor pulmonale.