Pulmonary Regurgitation Flashcards
What is physiological regurgitation?
Minor or trace degrees of regurgitation (in otherwise normal heart)
What is pathological regurgitation?
Regurgitation caused by disease (abnormal degree of regurgitation)
What is organic PR?
Primary anatomical problem with the valve structure - abnormalities of the valve itself (intrinsic PV disease)
What is functional PR?
Occurs secondary to causes other than primary valve problem (e.g. diseases affecting RV and MPA leading to annular dilatation, but the PV is anatomically normal)
Common causes of functional PR?
- Pulmonary HTN
- PA dilatation
- RV infarct
- Congenital heart disease
- RV cardiomyopathy
Common causes of organic PR?
- Infective endocarditis
- Congenital lesions (e.g. post Tetralogy of Fallot repair)
- Iatrogenic causes (e.g. post pulmonary valvotomy)
- Other rare causes: trauma, carcinoid syndrome, rheumatic involvement
What are the Doppler clues to significant PR?
- Colour jet width
- CW intensity of PR signal
- Rapid deceleration slope
- Early termination of PR signal
- Diastolic flow reversal in branch PA
Significance of colour jet width in assessing PR severity?
- How much of RVOT PR jet occupies during diastole
- Wider PR jet = worse PR
- Jet to annulus ratio
- Vena contracta width
How to assess jet to annulus ratio in PR, and its significance?
- Jet:annulus = B/A
- A = PV annulus measured at hinge point (onset of QRS complex)
- B = jet width measured at same level as RVOT (onset of QRS)
- Severe PR when jet:annulus ratio ≥ 50%
What three regions need to be seen to accurately measure VC-W?
- Flow convergence
- Vena contracta
- PR jet
What is the vena contracta?
- Narrowest neck of flow region at level of PV immediately below flow convergence area
- Measured PSAX for PR: early to mid-diastole
Significance of VC-W in PR?
- Limitation: significance of VC-W yet to be defined
Significance of intensity of CW PR signal in assessing PR severity?
Stronger signal = more severe regurgitation = more RBCs moving
Mechanism of CW mild PR trace?
- PAEDP is high whilst RVEDP is low
- As diastole progresses, diastolic gradient decreases as PA pressure declines and RV pressure rises as it fills with blood during diastole
Mechanism of CW severe PR trace?
- RVEDP rises rapidly due to rapid increase in RV diastolic volume caused by severe PR = rapid decline in pressure gradient
- PR signal can terminate before end-diastole meaning RV diastolic pressure = PV diastolic pressure (PR must be very severe)
Limitation of steep deceleration slope/early PR signal termination in severe PR?
- Seen due to elevated RVEDP
- RVEDP can also be elevated due to poor RV compliance
What is early PR signal termination?
Early PR termination if RV diastolic pressure = PV diastole pressure (PR needs to be very severe)
Significance of rapid deceleration slope in PR?
- Deceleration slope reflects pressure gradient between PA and RV in diastole
- Measured by p1/2t
- Severe PR when p1/2t < 100ms
- PR Index (PRi)
- Short slope and early termination of PR = marked elevation in RVEDP (could be due to severe PR or reduced RV compliance)
What is the PR index and what is its significance?
- PRi = B / A
- B = PR duration
- A = total diastolic period
- Severe PR when PRi < 0.77
Where is diastolic flow reversal seen in severe PR?
- Seen from level of PA branches; may be seen on CFI but best appreciated by PW (sample volume placed within LPA/RPA)
- Severe PA => diastolic flow reversal in RPA/LPA
Doppler characteristics of “free PR”?
- Short duration, low velocity jet (easily missed by CFI)
- Should be identified by CW Doppler
What pressures can be derived from PR signal?
- Mean PAP
2. PAEDP
Formula to calculate PAEDP?
- PAEDP = 4V(end-PR)^2 + RVEDP
- In the absence of TS, RVEDP = RAP
Formula to calculate mPAP?
- mPAP = 4V(early-PR)^2 + RAP
