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Right Ventricular Failure
Part 1
Education>Expert TEE>Right Ventricle>Right Ventricular Failure>1
Right Ventricular Failure
 
Right ventricular failure is associated with a poor outcome.  Right ventricular failure can be caused by right ventricular infarct/ischemia, pulmonary hypertension, cardiomyopathy, or congenital defects.  The right and left ventricles are sensitive to the other's pathologic conditions such that the diseased chamber can affect the function of the normal chamber. 

Ventricular interdependence is affected by the pericardium, the interventricular septum, and the pulmonary vasculature.  Impaired function in one chamber can mechanically interfere with the filling of the other ventricle.  The pericardium enhances ventricular interdependence.  Right ventricular failure may cause septal shifts once pericardial constraint exceeds right ventricular compliance.  Similarly, left ventricular dysfunction may impair right ventricular filling thru septal shifts. 

As the right ventricle begins to fail, its output and left ventricular preload begin to fall.  In the absence of left ventricular dysfunction, the right ventricle becomes dilated and hypokinetic/akinetic while the left ventricle becomes hypovolemic and left ventricular cardiac output falls. 
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Right Ventricular Failure
with IVS Shift
2D/M Mode
Qualitative Assessment of Systolic Function
 
The right ventricle's main function is a volume pump whereas the left ventricle functions as a pressure pump.  The thin-walled right ventricle is sensitive to changes in afterload (pulmonary artery pressure).  An increase in afterload may result in a marked decrease in right ventricular function.  The preload, afterload, and intrinsic right ventricular function are all interrelated in the function of the right ventricle.   Qualitative assessment of the systolic function of the right ventricle is determined by the motion of the free wall of the right ventricle and the septal wall displacement and motion.  Many factors can affect the septal wall motion so the motion of the right ventricular free wall is a more reliable indicator of right ventricular systolic function.  Right ventricular wall function is determined by wall motion and wall thickening.
 
Quantitative assessment is a tedious and time-consuming task and is usually not done clinically.  Clinically, qualitative assessment is the usual assessment of right ventricular function.
Wall Motion
 
Wall motion abnormalities of the free wall of the right ventricle are graded as normokinetic, hypokinetic, akinetic or dyskinetic.  The grading system of hypokinesis utilized to describe left ventricular wall motion abnormalities is not used in right ventricular hypokinesis.  Different gradations of hypokinesis are very difficult to diagnose because right ventricular wall motion is very load dependent. 

The right ventricle is a very compliant chamber that is relatively insensitive to changes in preload.  The response to increases in preload is right ventricular dilation, but wall motion is normal.  As the right ventricle continues to dilate, eventually the pericardium will restrain the right ventricle and compliance of the right ventricle quickly falls.  Further increases in preload will cause wall motion abnormalities, septal shifts, and tricuspid regurgitation. 

The right ventricle is much more sensitive to changes in afterload than the left ventricle.  Since the right ventricle is a volume pump, acute increases in afterload (pulmonary hypertension) may cause right ventricular dysfunction.  The right ventricular free wall becomes hypokinetic or akinetic. Right ventricular dysfunction is characterized by the RVEDD being larger than 3 cm and the RV FAC is less than 25%.
RV Wall Motion Abnormalities
Normokinetic
Hypokinetic
Akinetic
Dyskinetic
 
 
RV Dysfunction
RVEDD > 3 cm
RV FAC < 25%
 
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Normokinesis Hypokinesis Akinesis
Wall Thickness
 
The right ventricular free wall thickness is normally less than 1/2 of the left ventricular free wall thickness.  In end-diastole, the right ventricular free wall is normally less than 5 mm.  The right ventricular inflow is trabeculated posteriorly and inferiorly.  The RVOT is smooth and has no trabeculations.
 
If the right ventricular thickness is greater than 6 mm then hypertrophy (RVH) is present.  In long-standing pulmonary hypertension, the right ventricle hypertrophies to more than 10 mm when cor pulmonale is present. 
Right Ventricular Length and Area
 
Normally, the right ventricular area (RVA) is equal to 0.6 of the left ventricular area (LVA).  Also, the right ventricular length (RVL) is 0.6 of the left ventricular length (LVL).  On the ME4CV, the right ventricular apex (RV Apex) is proximal to the left ventricular apex (LV Apex). 
RV and LV Area and Legth
   
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Right and Left Ventricular Length Right and Left Ventricular Area
 
 
Measurement Reference
Range
Mildly
Abnormal
Moderately
Abnormal
Severely
Abnormal
Basal RV Diameter (TVA) 2.0-2.8 2.9-3.3 3.4-3.8 >3.8
Mid RV Diameter 2.7-3.3 3.4-3.7 3.8-4.1 >4.1
Base-to-Apex RV Diameter 7.1-7.9 3.4-3.7 3.8-9.1 >9.1
RVOT (Above Aortic Valve) 2.5-2.9 3.0-3.2 3.0-3.5 >3.5
PVA Diameter 1.7-2.3 2.4-2.7 2.8-3.1 >3.1
Pulmonary Artery Diameter 1.5-2.1 2.2-2.5 2.6-2.9 >2.9

 
Interventricular Septal Shape and Motion
Normal
 
Septal motion is determined by the depolarization pattern of the myocardium, the transeptal pressure gradient, and the presence or absence of septal ischemia.  Normally, the depolarization pattern of the heart is centered on the left ventricle because of its increased mass compared to the right ventricle.  The conduction of the left bundle proceeds the conduction of the right bundle by 10-20 milliseconds.  The conduction pattern results in the activation of the left side of the interventricular septum first, followed by sequential depolarization of the left and right ventricles.  Normally, the pressure of the left ventricle exceeds the pressure of the right ventricle and the septum is not ischemic.  The septum is a convex structure and bows into the right ventricle.  Normal shape of the interventricular septum is to maintain a convex shape with the left ventricle throughout systole and diastole.

If the right ventricle hypertrophies, the mass of the right ventricle may equal or exceed the mass of the left ventricle.  The interventricular septum will flatten and exhibit paradoxical motion if the right ventricular mass exceeds the left ventricular mass.  The paradoxical motion is maximal at end-systole and early diastole when the peak systolic unloading of the right ventricle is maximal. Paradoxical motion is recognized by a concave shape of the left ventricle during systole and concave shape during diastole.

If the right ventricle dilates, the septal shape will appear to flatten during diastole when the right ventricular pressure exceeds the left ventricular pressure.  During systole, the convex shape is restored because the pressure gradients are restored.

The interventricular septum is the only section of the heart exposed to external pressures.  As the right ventricle contracts, the pressure of the right ventricle increases and its long and short axis decrease.    The net effect is for the interventricular septum to appear relatively hypokinetic when compared to the other walls of the heart.  The interventricular septum will thicken normally, buts its normal wall motion appears hypokinetic.  The septum can move normally and thicken normally also.
 
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Normal Septal Motion
(Relative Hypokinetic)
Normal Septal Motion
Concentric Hypertrophy
 
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ME 4CV ME RVIO mTG RVSAX
 
Right Ventricular Pacing
 
A right ventricular paced heart will exhibit early right ventricular depolarization followed by left ventricular depolarization.  In a non-paced heart, the left ventricle starts to depolarize prior to the right ventricle for a few milliseconds, followed by simultaneous left and right ventricular depolarization.  In the paced myocardium, the free wall and the interventricular septum depolarize first before the left ventricle depolarizes.  The net effect is for the septum to appear to bounce towards the right ventricle and then correctly contract (with a convex shape) in mid to late systole.   If the heart is paced externally with a pacing wire attached to the free wall of the right ventricle, the free wall will contract first, followed by the interventricular septum and then the left ventricle.  If the pacing wire is internal where the wire is attached to the apex of the right ventricle, then the interventricular septum contracts first, followed by the free wall and the left ventricle.
 
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Normal IVS RV Paced (External) RV Paced (Internal)
CVP Estimation
 
The CVP can be calculated from the IVC diameter and its response to respiration.  If the CVP is low (<  10 mmHg) then the IVC diameter will be small and it will change with respiration.  If the CVP is high (> 20 mmHg) then the ICV diameter will be large and it will not respond to respiration.  The chart on the right indicates the CVP with an IVC diameter and its variance with respiration.  The acoustic window for the IVC diameter located at the same level as a mid-esophageal view of the tricuspid valve or transgastric view of the mitral valve with the probe rotated to the far right or clockwise to view the IVC.  Sometimes the plane of the probe may have to be electronically rotated 10 to 20 degrees to find the IVC. 
CVP From Hepatic Vein Diameter
CVP
Right Ventricular Dysplasia
 
Right ventricular dysplasia is a condition where the free wall myocardium is replaced by adipose or collagen containing tissue.  Arrhythmia and sudden death can occur.  Right ventricular dysplasia can exhibit right ventricular enlargement, focal wall motion abnormalities, and aneurysms of the free wall.  The adipose infiltration appears brighter than other parts of the myocardium, similar to interatrial septal lipomatosus scans. 
 
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