14 Pulmonary valve disease Flashcards
What are the causes of PS?
RHD, IE, carcinoid, congenital, sub-valvular and supra-valvular obstruction and infundibular obstruction.
In rheumatic PS, bacterial infection causes inflammation. This causes fibrosis and scarring, and, therefore, thickening, calcification and commissural fusion, of the PV. This restricts PV mobility.
In IE, the bacterial infection causes vegetations on the PV which damage the leaflets.
In carcinoid PS, metastatic carcinoid tumours secrete serotonin causing fibrosis, calcification and thickening of the TV, and PV.
Congenital PS can be isolated (e.g. bicuspid TV or PV dysplasia) or part of a CHD (e.g. TOF).
RVOT obstruction due to fibromuscular PS or accessory muscular bands. PA obstruction due to William’s syndrome or surgery.
Infundibular obstruction involves blockage of the part of the RVOT at the PV.
What are the TTE characteristics of PS?
Thickened and calcified PV leaflets, restricted PV leaflets, decreased PVA, increased PV Vmax, and/or increased PV PG.
In rheumatic PS, there is commissural fusion.
In IE, there are vegetations.
In congenital PS, there is systolic doming of the leaflets.
In obstruction, there is narrowing with increased RVOT or PA velocity.
In infundibular obstruction, there is infundibular narrowing with possible infundibular hypertrophy.
What are the symptoms and signs of PS?
Fatigue, dyspnoea, presyncope/syncope, symptoms of RV dysfunction and/or symptoms of the underlying cause.
A wide split S2 and an ejection systolic murmur in the pulmonary area. RVH is a sign of severe PS.
What are the qualitative methods used to assess PS?
Peak velocity and peak gradient.
If the RVOT Vmax is <1m/s, use the simplified Bernoulli equation to calculate the PG, and if the RVOT Vmax is >1cm/s, use the full Bernoulli equation to calculate the PG.
∆P = 4 x V2
∆P = 4 x (V2/2 – V2/1)
What are the effects of PS on chamber size and function?
RV pressure overload, RVH, RV dilatation, RV systolic and diastolic dysfunction, RA dilatation, PA dilatation, TR, systolic IVS shift and LV dysfunction.
PS obstructs blood flow from the RV to the PA so increases RV afterload and causes RV pressure overload. This causes RVH. RVH causes RV diastolic dysfunction (increased RV stiffness decreases RV filling) which increases RA pressure. This causes RA dilatation. The increased RV pressure causes RV dilatation. This causes RV systolic function which decreases RVEF and causes right sided HF and its symptoms. The RVH impairs tricuspid leaflet coaptation and the RV dilatation causes tricuspid annular dilatation. This causes TR which causes further RA dilatation. PS causes turbulent blood flow in the PA which causes post-stenotic PA dilatation. The increased RV pressure causes the IVS to shift to the left during systole. This can decrease LV systolic and diastolic function. In severe chronic PS, the decreased RV CO can decrease LV filling which decreases LV SV and LV CO. This can cause LV systolic and diastolic function.
What are the causes of PR?
RHD, IE, carcinoid, congenital and secondary.
In rheumatic PR, bacterial infection causes inflammation. This causes fibrosis and scarring, and, therefore, thickening, calcification and commissural fusion, of the PV. This impairs coaptation.
In IE, the bacterial infection causes vegetations on the PV which damage the leaflets.
In carcinoid TS, metastatic carcinoid tumours secrete serotonin causing fibrosis, calcification and thickening of the TV, and PV which impairs coaptation. .
Congenital PS can be isolated (e.g. bicuspid TV or PV dysplasia) or part of a CHD (e.g. TOF).
The causes of secondary PR include valvuloplasty (pulmonary annular dilatation and leaflet tearing) and TOF repair.
What are the TTE characteristics of PR?
Thickened TV leaflets, impaired PV coaptation, diastolic regurgitant flow.
In rheumatic PR, there is commissural fusion and mild central PR.
In IE, there are vegetations and severe eccentric PR.
In carcinoid PR, there is plaque and severe eccentric PR.
In secondary PR, there is pulmonary annular dilatation or absent or abnormal PV function.
What are the symptoms and signs of PR?
Fatigue, dyspnoea, palpitations, syncope and/or oedema.
Oedema, jugular venous distention, cyanosis, hepatomegaly, pulmonary ejection click, Graham steell murmur, RV heave, quiet or absent S2 and/or wide pulse pressure.
What are the qualitative methods used to assess TR?
PA diastolic flow reversal.
What are the quantitative methods used to assess TR?
PR jet width to RVOT diameter, vena contracta to PV annulus percentage or by 3D, PHT, DT, PR index.
How are PR jet width to RVOT diameter and
RVOT VTI / LVOT VTI calculated for PR?
In RVOT outflow or PSAX, use colour M-mode, measure the PR jet width during diastole and RVOT diameter during systole and calculate the ratio (PR width /RVOT diameter).
In severe PR, the RVOT VTI / LVOT VTI is high.
How are PHT and DT affected in PR?
In severe PR, the PHT is fast/short.
In severe, PR, the DT is fast/short.
This is because, in severe PR, the PA pressure is high and the RV pressure is low so the PG is high at the start of diastole. The PR causes the PA pressure to decrease faster so the PA and RV pressures equalise faster.
How is the PR index calculated?
PR index = (PR duration) / (diastole duration)
In RVOT outflow or PSAX, use CWD, measure the PR duration (flow above the line) and the diastolic duration (flow above and on the line).
What are the effects of PR on chamber size and function?
RV volume overload, RV dilatation, RVH, RV systolic and diastolic dysfunction, RA dilatation, PA dilatation, TR, diastolic IVS shift and LV dysfunction.
PR causes RV volume overload which causes RV dilatation and later RV eccentric hypertrophy. This causes RV systolic dysfunction which causes right sided HF and its symptoms. The RV dilatation causes tricuspid annular dilatation which causes TR. The RV volume and pressure overload, and TR, causes RA dilatation. PR causes flow during diastole which causes PA dilatation. The RV dilatation and dysfunction causes the IVS to shift to the left during diastole. This decreases LV function which causes left sided HF and its symptoms.
