Right ventricular function assessment
Right ventricular systolic function examination methods
In contrast with the left ventricle it has thinner walls and it is more sensitive to changes in afterload (pulmonary artery pressure).
An increase in afterload may result in a decrease in right ventricular function.
The hemodynamic factors as preload, afterload, and intrinsic right ventricular function are all interrelated and they all have an impact in the function of the right ventricle.
Image 1 Normal RV chamber size parametres
Adapted from: Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of, Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2016 Apr;17(4):412. doi: 10.1093/ehjci/jew041. Epub 2016 Mar 15. Erratum for: Eur Heart J Cardiovasc Imaging. 2015 Mar;16(3):233-70. PMID: 26983884.
Image 2 Normal RV function values
Adapted from: Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of, Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging. 2016 Apr;17(4):412. doi: 10.1093/ehjci/jew041. Epub 2016 Mar 15. Erratum for: Eur Heart J Cardiovasc Imaging. 2015 Mar;16(3):233-70. PMID: 26983884.
1. Wall Motion
Wall motion of the free wall of the right ventricle can be described and then graded as normokinetic, hypokinetic, akinetic or dyskinetic.
The grading system of reduced wall motion called hypokinesis which is used to describe left ventricular wall motion abnormalities is not used in right ventricular hypokinesis. The system is not used due to the fact that right ventricular hypokinesis is very difficult to diagnose because right ventricular wall motion is very load dependent.
The right ventricle has a thinner wall and it is a compliant chamber which leads to it being relatively insensitive to changes in preload. When the preload increases the right ventricular responses by it’s dilation, but wall motion remains normal. Until when the right ventricle continues to dilate towards pericardium, eventually the pericardium restrains the right ventricle and compliance of the right ventricle suddenly falls quickly.
On the contrary the right ventricle is much more sensitive to changes in afterload than the left ventricle. Because the right ventricle works as a volume pump, acute increases in afterload (for example in pulmonary hypertension) may cause right ventricular dysfunction. The right ventricular free wall reduces it’s motion and becomes hypokinetic or akinetic.
VIdeo 1 Severe dysfunction of dilated RV
Video 2 Patient with ARVC: Dilatation and severe systolic dysfunction of the right ventricle, wide-open secondary tricuspid regurgitation - A4C, color
Video 3 Patient with acute pulmonary embolism and cor pulmonale: Dilatation and mild systolic dysfunction of the right ventricle, McConnel’s sign (hypokinesis of medial segments, normal kinetic of apical part of the right ventricle) - A4C
Video 4 Dilated and impaired systolic function of RV visible already in PLAX view
2. Wall Thickness
The right ventricular free wall thickness is considered normal when its dimension is less than 1/2 of the left ventricular free wall thickness.
In the end-diastolic phase of a cardiac cycle, the right ventricular free wall is normally less than 5 mm.
The right ventricular inflow tract is trabeculated posteriorly and inferiorly. The right ventricular outflow tract is smooth and has no trabeculations.
If the right ventricular thickness is greater than 6 mm then right ventricular hypertrophy is present.
In long-standing pulmonary hypertension, the right ventricle expands to more than 10 mm when chronic cor pulmonale is present.
Image 3 Normal wall thickness of RV = 5 mm
3. Right Ventricular Length and Area
Another way to assess right ventricular function is by measuring the right ventricular length and area and their ratio in comparison to left ventricle dimensions.
Image 4 Mildly dilated size of RV2 and RV3
Image 5 Patient with acute pulmonary embolism and cor pulmonale: Dilatation of the right ventricle - A4C
4. Interventricular Septal Shape and Motion
The motion of the interventricular septum is determined by the way and direction of depolarization of the myocardium, the pressure gradient across the interventricular septum, and the presence or absence of ischemia in the interventricular septum.
Normally, the pressure of the left ventricle is higher than the pressure of the right ventricle and so the septum is a convex structure and it is curved into the right ventricle maintaining a convex shape throughout the cardiac cycle.
In the case of right ventricle hypertrophy, the myocardial mass of the right ventricle is able to produce higher pressure becoming equal or even exceeds the pressure of the left ventricle. The interventricular septum either flatten and moves paradoxically if the right ventricular mass exceeds the left ventricular mass.
The paradoxical motion shows maximally at the end of systole and in the beginning of diastole. Paradoxical motion presents as a concave shape of the left ventricle during systole as well as during diastole.
In the case of right ventricle dilatation, the shape of the interventricular septum will appear to flatten during diastole when the right ventricular pressure exceeds the left ventricular pressure. Then over the systolic phase, the interventricular septum is convex because the pressure gradients are restored.
The interventricular septum is also exposed to external pressures of the body. The effect of external pressure for the interventricular septum is that it appears relatively hypokinetic in comparison to the other walls of the heart. The interventricular septum thickens normally, but its wall motion appears hypokinetic.
Video 5 D-shape of LV due to pressure overlad caused by dilation and dysfunction of RV
5. Tricuspid annular plane systolic excursion (TAPSE)
How is it acquired?
TAPSE uses measuring the anteroposterior excursion of the tricuspid free annulus during systole which is obtained from the apical 4 chamber view with an M-mode pick directed through the lateral tricuspid annulus.
Normal value of peak excursion is more than 17, <17 is considered pathologic.
Image 6 TAPSE measurement - Normal function of RV (TAPSE 30mm) - A4C
Image 7 Patient with dilatation and systolic dysfunction of RV (TAPSE 14mm) - A4C
6. Systolic excursion velocity – Tissue doppler imaging
How is it acquired?
This method uses an apical view in a form of the tissue Doppler gate placed on the lateral right ventricular wall about 1-2 cm above the tricuspid annulus.
The S’ wave represents the systolic velocity, which assesses the right ventricular longitudinal function.
S' corresponds to the peak of the positive inflection - normal S' >10 cm/s
Image 8 Normal systolic function of RV (Sm TDI 13mm) - A4C, tissue doppler
Image 9 Patient with ARVC: Dilatation and systolic dysfunction of RV (Sm TDI 5mm) - A4C, tissue doppler
7. Fractional area change
This method uses a two-dimensional measure of right ventricular global systolic function.
How is it acquired?
To evaluate the fractional area change the examiner traces the right ventricular endocardial border at end diastole and then at the end of systole.
After tracing the difference of the end-diastolic area and end-systolic area the result is divided by the area at end diastole. To calculate fractional area change use the formula below.
Formula: RV fractional area change = (end diastolic area – end systolic area) / end diastolic area
Image 10 Reference values for FAC
Image 11 Borderline systolic function of the left ventricle, FAC 34% - A4C (diastole)
Image 12 Borderline systolic function of the left ventricle, FAC 34% - A4C (systole)
Image 13 Patient with acute pulmonary embolism and acute cor pulmonale: abnormal FAC (26%) - A4C (diastole)
Image 14 Patient with acute pulmonary embolism and cor pulmonale: abnormal FAC (26%) - A4C (systole)
References
1. Bassem Sobhi Ibrahim. (2016, May 12). Right ventricular failure. Escardio.Org. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-14/Right-ventricular-failure
2. Arrigo M, Huber LC, Winnik S, Mikulicic F, Guidetti F, Frank M, Flammer AJ, Ruschitzka F. Right Ventricular Failure: Pathophysiology, Diagnosis and Treatment. Card Fail Rev. 2019 Nov 4;5(3):140-146. doi: 10.15420/cfr.2019.15.2. PMID: 31768270; PMCID: PMC6848943.
3. WEERAKKODY, Yuranga a David CARROLL. Right ventricular function (point of care ultrasound) [online]. [cit. 2021-8-1]. Dostupné z: https://radiopaedia.org/articles/right-ventricular-function-point-of-care-ultrasound?lang=us
4. DiLorenzo MP, Bhatt SM, Mercer-Rosa L. How best to assess right ventricular function by echocardiography. Cardiol Young. 2015 Dec;25(8):1473-81. doi: 10.1017/S1047951115002255. PMID: 26675593; PMCID: PMC4803295.
5. Right Ventricular Failure. (n.d.). © JLS Interactive, LLC. Retrieved October 1, 2021, from https://e-echocardiography.com/page/page.php?UID=1427192221
