The controversy of right ventricular systolic pressure: is it time to abandon the pulmonary artery catheter?

In this issue of Anaesthesia there are two papers that contribute to the growing controversy as to whether Doppler echocardiography can be used to diagnose pulmonary hypertension. Cowie et al. 1 and Soliman et al. 2 have sought to determine the role of transoesophageal echocardiography (TOE) in estimating right ventricular systolic pressure (RVSP) and systolic pulmonary artery pressure (sPAP), compared with the gold standard of pulmonary artery catheter measurements. Doppler echocardiography has been used to estimate sPAP since the early 1980s. Using transthoracic echocardiography (TTE), Skjaerpe and Hatle were the first to demonstrate that the peak velocity of blood flow across a tricuspid regurgitant jet could be used to estimate RVSP 3. Furthermore, Yock and Popp found a good correlation between the Doppler-derived estimates of RVSP and right heart catheter measurements (r = 0.93) 4. Subsequently, RVSP became an important echocardiographic parameter that was used by clinicians to estimate pulmonary artery pressures. However, it is important to discuss the clinical value and the accuracy of Doppler-derived estimates of RVSP. Although the early work from Yock and Popp 4 and Skjaerpe and Hatle 5 found a close correlation between the Doppler-derived RVSP and the measurements from direct right heart catheterisation, subsequent studies produced conflicting results 6, 7. In a recent meta-analysis, Taleb et al. 8 found a wide range of correlations between these two measurements; however, even in the studies with a high degree of correlation, the diagnostic accuracy (defined as the ability to predict sPAP within 10 mmHg of the value measured by right heart catheterisation) was only in the range of 75–78%. While overall Doppler echocardiography is a fairly sensitive indicator of pulmonary hypertension (sensitivity 88%), the specificity is low (56%) 8. Consequently, most current guidelines recommend that outpatient Doppler echocardiography should be used as a screening tool for pulmonary hypertension, whilst the definitive diagnosis should be reserved for right heart catheterisation 9, 10. The next reason for the controversy is a question of measures. Traditionally, pulmonary hypertension is defined by a mean pulmonary artery pressure (mPAP) > 25 mmHg. This value is either measured directly during right heart catheterisation or calculated from the peak systolic and diastolic pulmonary artery pressures. The RVSP, however, is an estimation of sPAP and not mPAP. There are several ways of estimating mPAP using echocardiography. Most commonly, mPAP can be assessed by using the peak velocity of a jet of pulmonic insufficiency. This parameter, however, is rarely obtained in clinical practice because most patients do not have sufficient pulmonic insufficiency to allow a complete Doppler envelope. With mixed results, several authors have used other methods of estimating mPAP from Doppler TTE 11-13. None of these alternative techniques have made it to the mainstream echocardiography laboratory. The last aspect of this controversy is a problem of semantics. The World Health Organization (WHO) and the American College of Chest Physicians make a clear distinction between pulmonary hypertension and pulmonary arterial hypertension 9, 10. WHO group 1 pulmonary hypertension, formerly known as primary pulmonary hypertension, is a disease of the pre-capillary pulmonary vasculature resulting in pulmonary arterial hypertension. The diagnosis of pulmonary arterial hypertension requires not only a mPAP > 25 mmHg, but also a pulmonary capillary wedge pressure or left atrial pressure (LAP) < 15 mmHg, and a pulmonary vascular resistance (PVR) > 3 Wood units. Furthermore, with WHO group 2 pulmonary hypertension, pulmonary artery pressures are elevated due to post-capillary hypertension or pulmonary venous congestion, usually from left-sided disease such as mitral stenosis, mitral regurgitation or left ventricular diastolic failure. The distinction between pulmonary hypertension and pulmonary arterial hypertension is important because although left-sided heart disease is the most common cause of pulmonary hypertension, only pulmonary arterial hypertension will respond to afterload reduction with a pulmonary vasodilator 9. In other words, an elevated RVSP found by TOE in the operating theatre may represent pulmonary hypertension, but if that pulmonary hypertension is caused by pulmonary venous congestion from severe left-sided disease, then the addition of pulmonary vasodilators would be of little value. Echocardiography yields clues to the presence of left-sided disease and there are echocardiographic means of estimating both LAP 14 and PVR 15, 16. Recent studies, however, have shown that intra-operative echocardiographic estimates of LAP are not accurate enough to be clinically useful 17, 18. Consequently, the diagnosis of true pulmonary arterial hypertension cannot be made on the estimation of RVSP alone. The majority of the previously discussed studies compared Doppler-derived RVSP and right heart catheterisation in outpatients, using TTE. Because of the close proximity of the oesophagus to the heart, the major advantage of TOE is the ability to capture high-resolution images. The disadvantage of TOE, however, is the limited ability to manipulate the angle of the interrogating Doppler beam. This is important for the estimation of RVSP because the accuracy of Doppler echocardiography depends upon a near-parallel alignment of the ultrasound beam and the direction of blood flow being measured. Misalignment of more than 20-30° will lead to gross underestimation of blood flow velocities and pressure gradients. The advantage of the studies of Cowie et al. 1 and Soliman et al. 2 over prior TTE studies is that the TOE was performed in the operating theatre with simultaneous pulmonary artery catheter readings, while the majority of TTE studies compared measurements that were taken hours and sometimes even days apart 8. The sPAP is dependent on cardiac output, and the variation in cardiac output over time could easily account for the reported discrepancy between RVSP estimates and direct right heart catheter measurements in these studies. The calculation of RVSP also depends upon an accurate estimate of right atrial pressure. Echocardiographic estimations of right atrial pressure are often inaccurate 19 and this may account for the majority of the error in RVSP estimation 6. Cowie et al. 1 and Soliman et al. 2 used direct central venous pressure measurements as their real-time estimate of right atrial pressure. This method avoids the error of right atrial pressure estimation inherent in the prior TTE-based studies. With simultaneous measurements and accurate estimation of right atrial pressure, it is surprising that these two studies have opposite results. Cowie et al. 1 found that the measurement of RVSP was achievable in 100% of their patients, and that it correlated closely with pulmonary artery catheter-derived parameters of sPAP (r = 0.98). In addition, there was a very narrow limit of agreement (–5 to +5 mmHg) across a wide range of pulmonary pressures. On the other hand, Soliman et al. 2 found that adequate Doppler signals were only acquired in 56% of their patients, and that Doppler-derived measurements were accurate (within 10 mmHg of pulmonary artery catheter measurements of sPAP) only 75% of the time. Part of the discrepancy between these two studies may be explained by different methodological approaches. Cowie et al. 1 measured the correlation between RVSP and sPAP, while Soliman et al. 2 evaluated the accuracy or the ability of RVSP to predict sPAP within 10 mmHg. It is certainly possible that two variables can correlate closely but not agree. An example of this would be the close correlation between systolic blood pressure and mean arterial pressure. These two measures correlate because one is dependent on the other, but their values are different. A similar discrepancy between correlation and accuracy has been described in the TTE studies of RVSP reported over the last 40 years 7, 8. In addition, these two studies had vastly differing success rates in obtaining adequate RVSP estimations (100% vs 56%). Both groups used multiple TOE views to look for optimal alignment of the tricuspid regurgitant jet. Soliman et al. 2 defined an adequate tricuspid regurgitant jet as having < 20° alignment with the Doppler beam, but misalignment was never a cause for exclusion in their study. Instead, the most frequent cause of inadequate Doppler signal was the lack of complete tricuspid regurgitant jet envelope. By definition, this approach automatically excludes patients with trivial tricuspid regurgitation, as the inability to produce a complete Doppler envelope is what distinguishes trivial from mild tricuspid regurgitation. The 56% success rate found by Soliman et al. 2, however, is in close agreement with previous work by Taleb et al. 8, who found that adequate Doppler signals for RVSP estimation could only be obtained in 52% of patients overall. Cowie et al. 1 did not specify how they determined an adequate Doppler tricuspid regurgitant jet signal. Despite all the controversy surrounding Doppler-derived estimates of RVSP, even those that argue against its accuracy acknowledge that the estimation of RVSP in clinical practice should not be abandoned 7, 20. Because of the non-invasive nature of TTE, the biggest risk involved in the estimation of RVSP is the risk of misinterpretation. It is for this reason that TTE-derived RVSP is often the only measure of pulmonary artery pressure to which outpatient clinicians have access. Although TOE is certainly more invasive than TTE, its use during cardiac surgery is becoming a part of routine practice. In the operating theatre and in the intensive care unit, TOE measurements of RVSP may be an important screening tool for pulmonary hypertension, particularly if this information is combined with the patient's history and other echocardiographic findings such as right ventricular hypertrophy and dysfunction, left ventricular diastolic failure, and/or valvular disease. Estimation of sPAP can be confirmed using pulmonary artery acceleration time, a measure of pulmonary haemodynamics that is completely independent of the tricuspid transvalvular gradient and can therefore be calculated in the setting of inadequate tricuspid regurgitation 21. There are many causes of pulmonary hypertension; however, an elevated RVSP finding during TOE examination does not provide a definitive diagnosis. A patient with an elevated RVSP in the setting of sepsis, may have elevated sPAP due to increased cardiac output that may not represent pulmonary arterial hypertension. A patient with severe mitral regurgitation may have elevated RVSP but mitral valve repair is more likely to improve their pulmonary haemodynamics than an intra-operative administration of pulmonary vasodilators. On the other hand, a patient with idiopathic pulmonary fibrosis may benefit from these therapies because their elevated RVSP represents true pulmonary arterial hypertension. The benefit of the pulmonary artery catheter in these complex patients is that pulmonary artery pressure trends can be monitored during surgery and into the immediate post-operative period. The placement of a pulmonary artery catheter may not be necessary in patients with normal biventricular function undergoing cardiac surgery. In complex patients, however, with known pulmonary hypertension, severe right or left ventricular dysfunction, or severe valvular disease, the pulmonary artery catheter and the TOE provide complimentary information. Accordingly, both monitoring modalities still hold a valuable place in the cardiac operating theatre. No external funding and no competing interests declared.

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