Assessment of pulmonary artery pressure (PA pressure)
The systolic PA-pressure (PASP) is an indicator of cardiac hemodynamic status and can be quiet accurately
non-invasively assessed with echocardiography. There are several pitfalls that may produce over- and
The PASP at rest is also an independent predictor of prognosis and an indicator for elevated left ventricular
filling pressures [Lam CS et al. 2009].
During exercise, and already at low stages (through 125 Watt), it can raise over 40 mmHg in 10 % of healthy persons under the
age of 60 years. In 30 % of healthy family members with genetic predisposition to pulmonary arterial hypertension (I/FPAH), it
can also rise over 40 mmHg at the same conditions [Grünig E et al. 2009].
Following animations show pathophysiological aspects of PA-pressure behavior.
Worst case scenario (pulmonary edema)
LV filling pressures rise rapidly and considerably, for example in case of acute onset atrial fibrillation in
the presence of LV diastolic dysfunction. Pressure at the end of LV diastole raises, retrograde raises the mean
atrial pressure and consequently the pressure in the pulmonary veins. When hydrostatic pressure in the lung
capillary vessels rises over 25 mmHg an acute pulmonary edema develops [Lindsey AW & Guyton AC 1959].
However, human body has safety mechanisms that can avert such situations, similar to the one showed in the next animation.
The Hermo-Weiler reflex
A reflex-like massive vasocons- triction of pulmonary arterioles develops in order to avoid that hydrostatic capillary pressure
raise up to dangerous limits.
An experimental left atrial (LA) hypertension was conducted with a balloon catheter occluding the mitral valve.
To a larger inflation followed a higher LA pressure and consequently a higher PA pres- sure.
The mechanisms for this reactive vasoconstriction remain unclear, however, it can at least partly
be counteracted with nitric oxide (NO) [Hermo-Weiler C et al. 1998].
The postcapillary pulmonary hypertension
Chronic changes of pulmonary vessels bed by sustained passive pulmonary hypertension in back pressure lead to
remodeling of the lung vessels.
A classic example is the mitral valve disease (stenosis and/or regurgitation) [Straub H.
Zur dynamik der klappenfehler des linken herzens. Deutsches Archiv für klinische Medizin 1917].
Assessment of PA-pressure is an important part of a correctly and comprehensive conducted echocardiographic
examination. Assessment of pulmonary artery systolic pressure (PASP) can be carried out by measuring
maximal tricuspid regurgitation velocity, and applying the modified Bernoulli equation to convert this value into
pressure values. Estimated right atrial pressure (RAP) must be added to this obtained value. Mean (PAMP)
and diastolic PA-pressures (PADP) can be estimated by assessment of the pulmonary regurgitation.
Normal values: rest up to 30 mmHg, during exercise up to 40 mmHg.
Mean PA-pressure (PAMP)
PAMP = pulmonary regurgitation gradient (M)
Normal values: rest up to 25 mmHg, during exercise up to 30 mmHg.
Diastolic PA-pressure (PADP)
PADP = pulmonary regurgitation gradient (D) + RAP
estimated RA-pressure is up to 5 mmHg, when inferior vena cava is < 20 mm and collapses at least 50 % in inspiration.
estimated RA-pressure can be 10, 20, 30 mmHg in case of absence of inferior vena cava collapse or
presence of a severe tricuspid regurgitation. Tricuspid velocities are slower in this case, comparison
to PAMP can be help- ful.