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Echocardiography 5 minutes before starting   Twitter

Cardiac function and PA pressure

—Echocardiographic examinations

—Cardiac function and PA pressure

Systolic LV function
Diastolic LV function
Longitudinal function
RV function
PA pressure

—Examples of pathological

Assessment of systolic pulmonary artery pressure (sPAP)

sPA is an indicator of cardiac hemodynamic status and porgnosis, and can be quiet accurately non-invasively assessed with echocardiography. There are several pitfalls that may produce over and underestimation:

Reliability of Noninvasive Assessment of Systolic Pulmonary ArteryPressure by Doppler Echocardiography Compared to Right HeartCatheterization: Analysis in a Large Patient Population, 2014

Prognostic relevance of elevated pulmonary arterial pressure assessed non-invasively: Analysis in a large patient cohort with invasive measurements in near temporal proximity, 2018

The sPAP 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].

Furthermore, the assessment of systolic pulmonary artery pressure during stress echocardiography has an inportant diagnostic and prognostic value:

Systolic pulmonary artery pressure assessed during routine exercise Doppler echocardiography: insights of a real-world setting in patients with elevated pulmonary pressures, 2018

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 Kitaev 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 severe chronic pulmonary hypertension

Chronic changes of pulmonary vessels bed by sustained passive pulmonary hypertension in back pressure lead to remodeling of the lung vessels. A similar picture can be seen in PAH and CTEPH.

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].

The current most common cause of persistent pulmonary hyper- tension is diastolic LV dysfunction [William P. Thompson & Paul D. White 1936].

Pulmonary artery pressure estimation

Assessment of PA-pressure is an important part of a correctly and comprehensive conducted echocardiographic examination. Assessment of systolic pulmonary artery pressure (sPAP) 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 (mPAP) and diastolic PA-pressures (dPAP) can be estimated by assessment of the pulmonary regurgitation.

Systolic PA-pressure (sPAP)

sPAP = tricuspid regurgitation gradient + RA-pressure (RAP)

sPAP = (Vmax² x 4) + RAP

Normal values: rest up to 35 mmHg, during exercise up to 40 mmHg.

Mean PA-pressure (mPAP)

mPAP = pulmonary regurgitation gradient (M)

Normal values: rest up to 25 mmHg, during exercise up to 30 mmHg.

Diastolic PA-pressure (dPAP)

sPAP = pulmonary regurgitation gradient (D) + RAP

Left: estimated RA-pressure is up to 5 mmHg, when inferior vena cava is < 20 mm and collapses at least 50 % in inspiration.

Right: 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.


© Derliz Mereles


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