It sounds to be a simple question . But, cardiology literature is sparse on the subject.
RV mimics a three dimensional triangular chamber .The inflow, body and outflow align themselves in complex planes .This makes measurement difficult.
What are the measurements to be made ?
- RV inflow tract (RVIT)
- RV body
- RV outflow tract (RVOT)
- RV Free wall thickness
How to measure RV size ?
- Inflow diameter is assessed in inflow view ( Para sternal long axis,probe tilted down towards lower sternal edge (cool . . .That is were tricuspid valve is located !)
- RV body can be assessed in long axis or 4 chamber view
- RVOT in short axis view.
What is the normal range ?
< 3 cm in parasternal long axis view
<8 cm Long axis ( RV apex to mid point of TV )
< 3- 4cm
RV outflow (RVOT)
1.8 to 3 cm
- All measurements are taken in end diastole .
- The largest diameter of RV is at its inflow(it is roughly equivalent to tricuspid annulus)
- RVOT size can vary , generally tapers as it reaches near the pulmonary valve .
How common is the differential RV enlargement*?
The complex shape and architecture of RV make the direction , sequence and magnitude of RV enlargement less predictable .
- Diastolic loading of RV generally have more uniform enlargement of RV .(Inflow, body, outflow )
- In dilated cardiomyopathy RV enlargement common in short axis > long axis
- Pressure over loading may not result in uniform enlargement as the pressure points on RV surface is not homogeneous.
- In congenital heart disease , RV shape and size depend more on the morphology(location of VSD, infundibular anatomy, muscle bundles, extent of trabeculations etc)
- In arrhythmogenic RV dysplasia (ARVD) outflow tract enlargement is more dominant.
* The fact that , RV can enlarge in focal and localised manner make it mandatory to measure RV dimension in multiple views and in all possible diameters.
At what pressure RV begins to enlarge ?
RV is believed to enlarge at > 60mmhg .Hypertrophy is usually precedes dilatation .
At what volume overload RV begins to enlarge ?
Our experience with ASD indicate when the pulmonary blood flow is twice that of systemic blood flow RV is distinctly enlarged. May be it begins to enlarge at> 1.5: 1 shunt
RV begins to enlarge horizontally or longitudinally ?
this aspect is not studied much. Generally volume overload causes more uniform enlargement.
How does acute RV enlargement differ from chronic RV enlargement ?
Dilatation is more conspicuous in acute RVE ( Pulmonary embolism, RV infarct ) associated wall motion defects and thinning favors acute RVE.
Normal or increased thickness is expected in chronic RV enlargement
Here is a five-star rated article on RV dimension
Published in 1986 , still considered a land mark paper . . .