Abstract
The echocardiographic assessment of pulmonary hypertension must include an appreciation of the interaction between the load imposed on the ventricle by the increased resistance of the pulmonary arteries and the contractile force of the right ventricle (RV). It is a combination of these two factors that determine the right ventricular and pulmonary artery pressures. Thus, an echocardiographic assessment must include assessment of both the pulmonary arterial load and the RV function. This chapter reviews the echocardiographic tools available for assessing both arterial load and function and the interaction between the two.
Keywords
echocardiography, pulmonary hypertension, pulmonary vascular function, pulmonary vasodilators, right heart failure, RV function, tricuspid regurgitation
Introduction
The echocardiographic assessment of pulmonary hypertension (PH) must include an appreciation of the interaction between the load imposed on the ventricle by the increased resistance of the pulmonary arteries and the contractile force of the right ventricle (RV). It is a combination of these two factors that determines the right ventricular and pulmonary artery pressures ( Fig. 36.1 ). Thus, the first principle is that an echocardiographic assessment must include assessment of both the pulmonary arterial load and the RV function.
The second principle is that the interaction between pulmonary vascular load and cardiac performance is not constant but rather is marked by differing phases as PH progresses. In early disease, RV contractility increases to compensate for the increase in pulmonary vascular resistance (PVR). This phase is marked by increased pulmonary artery pressures, maintained cardiac output, and few or no symptoms. Then there is a stage where the RV contractility is no longer able to compensate for the increase in PVR; the cardiac output starts to fall and progressive symptoms develop. At first, these occur only during exertion, so measures appear reasonably compensated when measured at rest. Finally, there is a completely decompensated phase in which reduction in RV function is so significant that cardiac output falls even under resting conditions. This results in a fall in pulmonary artery pressures despite the continued increase in PVR ( Fig. 36.2 ).
Thus, the echocardiographic assessment that follows will describe measures that assess pulmonary vascular load, measures of RV function, and some measures that attempt to quantify RV/pulmonary arterial coupling; that is, the degree to which the RV is compensating for the increase in load.
Assessment of Right Ventricle Afterload/Pulmonary Vascular Function
Pulmonary Artery Systolic Pressure
Pulmonary artery systolic pressure (PASP) can be reliably estimated from a continuous-wave Doppler assessment of the tricuspid regurgitation (TR) jet ( Fig. 36.3 ; Bernoulli equation; 4 × TR velocity = max pressure gradient) and has been validated in numerous studies. As Doppler intercept angle affects the measurement, multiple acoustic windows should be interrogated. Saline or contrast enhancement also should be available ( Fig. 36.4 ) to increase the intensity of the regurgitant signal and the sensitivity of results.
The regurgitant velocity represents the pressure gradient between the RV and right atrium. Thus, it measures RV systolic pressure (RVSP) minus the right atrial pressure (RAP). To use this clinically, an estimate of RAP can be made (see below) and then RVSP = 4 × TR velocity + RAP. The RVSP is equivalent to PASP, except when there is a significant gradient across the right ventricular outflow tract (RVOT) or pulmonary valve. Thus, in pulmonary stenosis, the systolic gradient would need to be considered when estimating PASP.
The other setting in which the Bernoulli equation needs to be used with caution is in severe TR. The early equalization of pressures between the RV and RA can result in considerable underestimation of PASP.
Diastolic Pulmonary Artery Pressure
Diastolic pulmonary artery pressure (dPAP) is calculated from a measurement of the peak velocity of pulmonary regurgitation (PR) at the end of diastole. This usually occurs simultaneously with the Q wave of the electrocardiogram (ECG) and after a small “notch” that reflects atrial contraction ( Fig. 36.5 ).
dPAP = 4 ( V PR end − diastole ) 2 + RAP
Mean Pulmonary Artery Pressure
Mean pulmonary artery pressure (mPAP) can be calculated using a number of methods:
- 1.
The Chemla formula that is derived from linear regression of the reasonably consistent relationship between PASP and mPAP. Thus, PASP can be measured from the maximal tricuspid regurgitant velocity, as depicted in Fig. 36.3 , and then mPAP is calculated using the formula: mPAP = 0.61∗PASP + 2 mm Hg.
- 2.
An average of all instantaneous pressure estimates, which is obtained by tracing the maximal instantaneous velocities across the TR regurgitant signal and averaged. The RAP pressure estimate is again added ( Fig. 36.6 ).
FIG. 36.6
Estimation of mean pulmonary artery pressure (mPAP). The tricuspid regurgitation time-velocity integral can be traced to determine the mean RV-RA gradient to which an estimate of RAP is added. RA , Right atrium; RAP , right atrial pressure; RV , right ventricle.
- 3.
Deriving PASP and dPAP using the methodologies stated above and incorporating these values into the formula: mPAP = ⅓ PASP + ⅔ dPAP.
The Right Atrium and Right Atrial Pressure
The right atrial size is traced from the RV apical view. The transducer should be rotated to ensure that the RA is as elongated as possible. This may require a different acquisition from that used to measure the left atrium. Recent guidelines have proposed the area–length measurement, with body surface area (BSA)–indexed values of 25 ± 7 mL/m 2 and 21 ± 6 mL/m 2 representing the average upper limit of normal measures for males and females, respectively.
RAP is typically estimated based on dimensions of the inferior vena cava (IVC). IVC measurements are made from the subcostal view, 1–2 cm from the junction of the right atrium (from a long-axis view). The maximum dimension can be measured from M-mode or 2D. IVC distensibility is calculated in response to respiratory measures that alter intrathoracic pressure; 50% collapsibility provides optimal sensitivity and specificity for detecting RAP greater or less than 10 mm Hg, but RAP is often underestimated when values exceed 12 mm Hg. Values are as follows ( Fig. 36.7 ):
- •
IVC <2.1 cm and collapsible >50%, RAP∼ 3 mm Hg.
- •
IVC >2.1 cm and collapsible >50% or IVC < 2.1 cm and collapsible ≤ 50%, RAP∼ 8 mm Hg.
- •
IVC >2.1 cm and collapsible <50%, RAP∼ 15 mm Hg.
Velocity-time integrals (VTIs) of the hepatic veins (or superior vena cava) provide an indication of elevated RAP. Hepatic vein systolic filling fraction (VTI systolic/VTI systolic + VTI diastolic) can provide semiquantitative assessment of RAP, with a measurement of <55% predicting RAP >8 mm Hg with good sensitivity and specificity. This technique offers advantages over IVC measurements in patients with falsely elevated IVC diameters (athletes, large BSA, and mechanically ventilated patients).
Other Measures of Right Ventricle Afterload
Pulmonary Arterial Acceleration Time
Pulmonary arterial acceleration time (PAT) is calculated via pulsed-wave Doppler, at the level of the pulmonary valve leaflets. Acceleration time is measured along the modal velocity from the baseline to peak ( Fig. 36.8 ). This method is less reliable than other methods of assessing PASP and is heart-rate dependent. It should not be applied when the heart rate is outside the range of 60–100 bpm. PAT <100 ms has been proposed to indicate a PASP >38 mm Hg (normal PAT is >120 ms)
Notching of the Right Ventricular Outflow Tract Signal
A qualitative measure of pulmonary arterial hypertension (PAH) is “notching” of the RVOT signal (see Fig. 36.8 ), although its absence cannot “rule-out” PH. This can give us insight into the underlying physiology of the PH. In large artery stiffness, an early notch relates to a restricted vascular bed, whereas a late notch could imply secondary PH due to left heart disease.
Echocardiographic Estimates of Pulmonary Vascular Resistance
PVR is calculated as the pressure gradient across the pulmonary vasculature (mPAP—left atrial pressure [LAP]) divided by cardiac output. Each of these factors can be estimated by echocardiography. In the absence of shunts, cardiac output can be measured using the left ventricle (LV) or RV as these should be equal. However, often the VTI of the RV outflow tract is used ( Fig. 36.9 ). Abbas et al. estimated PVR as PASP/RVOT VTI , but a very significant limitation of this formula was that the heart rate was ignored, which is a problem when one considers that heart rate represents the most important means of augmenting cardiac output. Thus, Haddad et al. improved this formula with the addition of heart rate (PVR = PASP/[HR × TVI RVOT ]) so that the calculation more closely approximates the pulmonary pressure gradient divided by cardiac output.
The other big limitation in applying these formulas to estimate PVR is that LAP is ignored. In situations in which LAP is elevated, these formulas will grossly overestimate PVR.
Defining Pre- Versus Postcapillary Pulmonary Hypertension
Echocardiography can be used to aid with the differentiation of precapillary (PAH) versus postcapillary PH. The current clinical standard requires right heart catheterization and the estimation of LAP by means of the pulmonary artery occlusion pressure (PAOP), which is otherwise known as the pulmonary capillary wedge pressure (PWCP), with values >15 mm Hg suggesting that PH is consistent with a diagnosis of raised LAPs due to left heart disease. There have been a number of attempts to develop a noninvasive estimate of LAP to assist in identifying those patients with precapillary (Class I PAH) or postcapillary (Class II PH due to left heart disease) causes of raised pulmonary pressures. This is a critical distinction because pulmonary vasodilators have demonstrated efficacy in pre- but not postcapillary causes of PH. However, it is controversial as to whether echocardiographic surrogates have a role in clinical decision making. Given the significance of the outcomes, current recommendations would be that patients with elevated estimates of PASP on echocardiography should undergo right heart catheterization both to confirm the result and to assess the contribution from left heart disease.
Despite this, noninvasive estimates of PCWP have been proposed from measures of pulsed-wave mitral inflow, and tissue Doppler of the mitral septal annulus, using the formula:
PCWP = 1.24 ∗ E / e ‘ + 1.9
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