Feeds:
Posts
Comments

Posts Tagged ‘pulmonary vascular ressitance’

Measurement of pulmonary vascular resistance (PVR) is traditionally done by cardiac catheterization. It remains the (un)disputed gold standard, despite numerous assumptions, errors in measurement, and lack of reproducibility.

PVR by Echocardiography

Recently, echocardiographic calculation of PVR gained importance. Resistance is pressure divided by flow. Pressure is measured by Doppler, flow is measured by the cross-sectional area of RVOT times the TVI. We can arrive at PVR quickly. As simple as that.

Still, many institutions and purists ( Who have huge trust in cath derived, Oxygen diluted data) ) won’t accept this as standard . They fail to realise echo methodology carries less limitation, if not similar limitations as in traditional cath method. However, a significant advantage is, it is more real -time, can be repeated any number of times, and documents a baseline PVR, and at least is useful for follow-up.

There are two formulas used.

1.Abbas Formula

PVR = (TRV / RVOT VTI) × 10 + 0.16

2.Haddad formula :

PVR= (TRV²/VTI_RVOT)

*TRV = Tricuspid Regurgitation Velocity (m/s)

*RVOT VTI = Right Ventricular Outflow Tract Velocity Time Integral (cm)

Comparing Abbas vs Haddad

The Abbas formula is better validated and widely used in clinical practice, as it was specifically designed to correlate with catheter-based pulmonary vascular resistance measurements. It provides reasonably accurate estimates, especially for screening pulmonary hypertension, though it tends to under-estimate PVR at higher values (>8–10 Wood units).

In contrast, the Haddad formula ) is simpler but less rigorously validated and is more commonly applied in research settings focused on right ventricular-pulmonary artery coupling rather than direct PVR estimation.

Haddad’s method may be less reliable in patients with significant tricuspid or pulmonary valve abnormalities. Therefore, Abbas remains the preferred formula for routine clinical application. There is still hope to improve Haddad equation.

How to improve upon Haddad equation* ?

The Haddad equation for estimating PVR (TRV²/RVOT VTI) lacks calibration and overlooks key hemodynamic variables. It can be improved by introducing empirically derived correction factors to correlate with catheter-based values. Incorporating right atrial pressure (RAP), RV functional indices like TAPSE or RV strain, and adjusting for heart rate or rhythm variability can enhance accuracy. Averaging VTI across multiple cardiac cycles could also stabilize measurements. Additionally, machine learning on large datasets and AI-enhanced model could outperform the current linear Haddad formula for non-invasive PVR estimation.

* This is a fresh area of study , young fellows should come forward to do.

Final message

As discussed earlier, Abbas remains the preferred formula. But, the real issue is cardiologists refusing to accept any Echo-derived PVR and incorporate it, in the day to day practice. We have accepted EF % as the gold standard for LV function in spite of some serious lacunae. PVR carries the same story. Cath-derived data, in all likelihood, is enjoying pseudo-sanctity. It is time we should embrace one of these Echo formulas regularly and make life simple for both ourselves and the patients (who are often tiny babies or children). I think it can be done without compromise on scientific purity.

Reference

1.Haddad F, Zamanian R, Beraud AS, Schnittger I, Feinstein J, Peterson T, Yang P, Doyle R, Rosenthal D. A novel non-invasive method of estimating pulmonary vascular resistance in patients with pulmonary arterial hypertension. J Am Soc Echocardiogr. 2009 May;22(5):523-9. doi: 10.1016/j.echo.2009.01.021. Erratum in: J Am Soc Echocardiogr. 2010 Apr;23(4):376. PMID: 19307098.

2.Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol. 2003 Mar 19;41(6):1021-7. doi: 10.1016/s0735-1097(02)02973-x. PMID: 12651052.

Read Full Post »

PH is an important clinical cardio-pulmonary entity , which we confront day to day. Though the prevalence of PH in a community is just 1 % (25 times less than systemic hypertension) it deserves a special place as the diagnosis is more complex and outcome is often adverse.

The defining criteria , the classification, and grading of PH has always been a difficult and dynamic academic task .Right from WHO’s 1974 definition, we have 7 global symposiums , last one happened few months ago, in July 2024 in Barcelona.

We have made rapid strides in all aspects of PH right from molecular , genetic , imaging and therpeutics. Still, there is one important issue that has been overlooked for quiet some long. The concept of fitting PH in 5 groups based on etiology, though appear to simplify things, there is a significant flaw.

The overlaps in etiology

1.The group 1 contains the famous , (now obsolete entity of primary pulmonary hypertension) Idiopathic PH , meaning that we don’t know the cause of it or we have excluded all known causes. Meanwhile, group 5 also has set of conditions of PH of unknown or unclear etiology. So, a IPH of group one can migrate to either group 4 or group 5 or vice versa.

2.PH due to congenital heart disease can be in both Group 1 and 3

3.If you take PH due to some of the connective tissue order, I am sure, it can fall into any of the 5 groups

Suggestions for the next PH working group

It is desirable that the next working group should acknowledge existence of inter and intra group overlaps of PH in a more clear manner. Either we should take away the groupism or the current definition of group 5 need to be more elaborate . It says multi-factorial. Instead we can try to find what are the groups it is likely to have an overlap. Should we need another a sixth group ? GO-PH (Group overlapping PH)

There can also be a place for combined etiological-hemodyanmic classification . (Example : Group 1 .Pre capillary .Group 1 Intra-capillary as in PVOD) . CTEPH though essentially is a precap PH, the risk factors of CTEPH and HFpEF can be shared one, making it combined pre and post cap PH a distinct possibility. )

Final message

While the problem of groupism in PH exists, the issue of highest importance in PH is something different. This is more philosophical . We need to be very clear what we mean by Idiopathic. As physicians, we must realize how relative this terminology is . What is idiopathic in your hospital, (However big you are) may turn out to be a missed case of mixed connective tissue disorder or silent CTEPH detected only by V/Q scan or a dual energy CT or a rare case of PVOD by judiciously reading a pulmonary angiogram in a dedicated PH center.

*Also we must recall, statistically up to 80% of PH is due to left heart (This HFpEF stuff has jacked this incidence still more ) and lung disease. Our efforts and resources should be used judiciously for optimal diagnosis and management of common conditions first.

Read Full Post »