Echocardiography in the Patient with Right Heart Failure

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10 Echocardiography in the Patient with Right Heart Failure

Anjali Tiku Owens, Martin St. John Sutton

Basic Principles of Right Ventricular Imaging

Step-by-Step Approach

Step 1: Analysis of Right Ventricular Size

Key Points

• Obtain two-dimensional (2D) images utilizing parasternal, right ventricular (RV) inflow, apical 4-chamber, and subcostal views.

• The RV has a crescent shape, with no accurate geometric representation.

• Measure RV basal, midcavity, and longitudinal dimensions from the apical 4-chamber view (Figure 10-1).

• The upper reference limits for the RV are: basal dimension, 4.2 cm; midcavity, 3.5 cm; longitudinal dimension, 8.6 cm.

• Assess the size of the RV in relation to the left ventricle (LV) from the apical 4-chamber view.

• Normal size—RV smaller than LV and does not participate in forming the apex of the heart

• Mildly enlarged—RV size still smaller than LV size

• Moderately enlarged—RV size equal to LV size

• Severely enlarged—RV size bigger than LV size

• Measure right ventricular free wall thickness (Figure 10-2).

• Normal thickness—≤ 0.5 cm in the subcostal view

Figure 10-1 Schematic from the apical view of a normal heart showing measurement of RV basal, midcavity, and longitudinal dimensions (arrows).

(Courtesy of Ted Plappert.)

Figure 10-2 2D echocardiogram from the subcostal view of a normal heart (left panel) and the heart in a patient with RV hypertrophy (right panel) showing measurement of RV free wall thickness (arrows).

Step 2: Analysis of RV Volume and Systolic Function

Key Points

• For volume measurements using area-length and Simpson’s rule, assumptions of geometric shape are necessary and may not be accurate.

• Estimate RV systolic function qualitatively: normal, mildly reduced, moderately reduced, or severely reduced

• Estimate RV systolic function quantitatively using a combination of the following methods.

• Right ventricular fractional area change (RVFAC) can be calculated using the following formula:

Using the apical 4-chamber view with focus on the RV, trace the RV volume from the tricuspid annulus down the free wall to the apex and back along the septum; tricuspid leaflets, trabeculations, and chords are regarded as cavity. RVFAC = 35% is the lower limit of normal in reference studies.

• On RV tissue Doppler, normal pulsed wave Doppler peak velocity at the tricuspid annulus is greater than 10 cm/s.

• Tricuspid annular plane systolic excursion (TAPSE) can be calculated from the apical 4-chamber view using M-mode and 2D techniques (see “Measurement of Prognostic Echocardiographic Parameters” below).

• Radionuclide ventriculography has been utilized historically for comparison with newer methods. However, due to the unique shape of the RV, three-dimensional (3D) echocardiography and cardiac magnetic resonance imaging (MRI) are best suited for accurate assessments of volume and systolic function (RV ejection fraction [RVEF]). These methods can be time consuming and are not widely available.

Step 3: Evaluation of RV Wall Motion

Key Points

• Septal and free wall motion should be assessed in multiple 2D views, including parasternal short-axis, apical 4-chamber, and subcostal views.

• RV volume and/or pressure overload can cause septal wall motion abnormality.

• Pressure overload of the RV causes flattening of the interventricular septum as a result of an abnormal pressure gradient between the RV and the LV, in essence pushing the septum toward the LV during both in systole and in diastole (Figure 10-3). Normally, when viewed in the parasternal short axis, the LV has the appearance of a symmetrical O or “doughnut.” With RV pressure or volume overload, the septum is D-shaped.

• Volume overload of the RV results in flattening of the interventricular septum during diastole only.

• The degree of septal flattening correlates approximately with the severity of pulmonary hypertension.

• Free wall motion should be assessed for regional wall motion abnormalities suggestive of RV infarction versus global wall motion abnormality.

• Septal and free wall thickening and endocardial excursion should be examined in multiple 2D views.

Figure 10-3 2D echocardiogram from the parasternal short-axis view of the interventricular septum in a normal heart (top panels) and the heart from a patient with RV volume and pressure overload (bottom panels) during diastole (left panels) and systole (right panels). Note the D-shaped LV in the bottom panels, illustrating shift of the septum toward the LV.

Step 4: Evaluation of Tricuspid Valve Regurgitation

Key Points

• Tricuspid regurgitation often accompanies significant right heart dysfunction and should be assessed along with function of the RV (see Chapters 2 and 6).

• Interrogation of the tricuspid regurgitation jet using Doppler is used to calculate the estimated pulmonary artery systolic pressure (PASP) (see “Measurement of Prognostic Echocardiographic Parameters” below).

Identify the Cause of Right Heart Failure

RV Infarction

• RV infarction is relatively rare. The vast majority of RV infarctions occur in the setting of acute inferior myocardial infarction.

• Obtaining right-sided electrocardiographic (ECG) leads in acute inferior myocardial infarction often helps in making the diagnosis.

• The characteristic hemodynamic sensitivity to alterations in preload is a hallmark of RV infarction and impacts upon treatment strategies.

Step-by-Step Approach

Step 1: Assess LV Wall Motion and Systolic Function, and Look for Mechanical Complications of Myocardial Infarction

Key Points

• Often, the inferior wall motion abnormality is mild, with preserved overall LV function.

• Occasionally, a ventricular septal defect (VSD) resulting in left-to-right shunting, or papillary muscle rupture with severe mitral regurgitation, will complicate an inferior myocardial infarction. In these situations, RV dysfunction can be exacerbated by volume overload.

Step 2: Assess the Right Heart

Key Points

• Dilatation of the RV with global or regional wall motion abnormality is common.

• Acute RV dysfunction can be a result of true myocardial infarction, or more commonly, ischemia that improves in time with supportive care.

• Acute RV dysfunction and dilatation also occur with acute pulmonary embolism.

• Annular dilatation with secondary tricuspid regurgitation is frequently encountered.

• Occasionally, right-to-left shunting through a patent foramen ovale (PFO) will result in oxygen desaturation and clinical deterioration.

Pulmonary Arterial Hypertension

• There are many etiologies of secondary pulmonary hypertension (Box 10-1). When pulmonary hypertension is suspected, a detailed search for an underlying cause should be performed. This section refers specifically to the evaluation of pulmonary arterial hypertension.

• Chronic pressure overload of the RV resulting from high pulmonary vascular resistance (PVR) results in pulmonary hypertension.

• There are echocardiographic signs of pulmonary hypertension that can be helpful in making the diagnosis and assessing disease progression and response to treatment.

• Echocardiography can be used to estimate PASP, pulmonary artery diastolic pressure (PADP), and PVR noninvasively (see “Measurement of Prognostic Echocardiographic Parameters” below).

Box 10-1 Etiologies of Pulmonary Hypertension

• Diseases that cause elevated pulmonary venous pressure

• Acute and chronic pulmonary embolism

• Intrinsic lung disease

• Disorders that cause intracardiac shunting

• Primary pulmonary hypertension

Step-by-Step Approach

Step 1: Assess RV Size and Function

Key Points

• The RV initially enlarges and hypertrophies as a compensatory response to pressure overload.

• RV function is often preserved or hyperdynamic during this phase of disease and can be assessed using TAPSE and qualitative estimation.

• With progressive increase in RV afterload, the RV initially hypertrophies and then dilates and the normal tricuspid valve geometry is disrupted, resulting in tricuspid regurgitation and systolic dysfunction leading to RV failure (Figure 10-4).

Figure 10-4 2D echocardiogram from the apical 4-chamber view showing severe RV dilatation that is apex-forming and marked dysfunction typical of end-stage RV failure (left panel in diastole, right panel in systole).

Step 2: Look for Associated Right Heart Findings of Pulmonary Hypertension

Key Points

• Tricuspid regurgitation due to annular dilatation is common.

• Right atrial (RA) enlargement is often present.

• M-mode of the pulmonic valve reveals a diminished or absent a wave.

• M-mode of the pulmonic valve reveals midsystolic closure—the “flying W” sign (Figure 10-5).

• Doppler velocity curve of the RV outflow tract (RVOT)/PA has mid-systolic “notching” (Figure 10-6).

• The main PA may be enlarged (>2.5 cm) and should be measured from the left parasternal acoustic window if 2D image quality permits.

• There are septal wall motion abnormalities suggestive of RV pressure overload (described earlier in “Basic Principles of Right Ventricular Imaging”).

• Left heart filling abnormalities including reduced mitral valve E/A ratio can be seen.

• In cases of severe pulmonary hypertension and RA enlargement, stretching of the foramen ovale may result in a right-to-left shunt.

• In advanced cases of PA hypertension, a pericardial effusion can be seen. Because of elevated RV pressure and hypertrophy, frank tamponade rarely occurs.

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