Noninvasive estimation of pulmonary artery pressure

Noninvasive estimation of pulmonary artery pressure T h o m a s Zellers, MD, a n d H o w a r d P. G u t g e s e l l , MD From the Division of Cardiology, Department of Pediatrics, University of Virginia, Charlottesville

Pulmonary hypertension is a complicating feature of many conditions, notably congenital heart disease and respiratory disease. Measurement of pulmonary artery pressure is essential in the managemen t of certain forms of cardiac disease and may help determine prognosis. It may also indicate a need for either supplemental oxygen or ventilatory assistance in patients with respiratory disease. Although pulmonary artery pressure can be measured directly by means of a catheter introduced into the pulmonary artery, the procedure is associated with risk, expense, and discomfort; several noninvasive techniques haye therefore been proposed. We review the available methods of estimating pulmonary artery pressure and suggest a plan for evaluation of suspected pulmonary hypertension. HISTORY AND PHYSICAL EXAMINATION The symptoms of pulmonary hypertension are nonspecific and rarely give any clue as to its presence or severity. In children, symptoms of pulmonary hypertension are apt to be ol~scured by those of the underlying cardiac or respiratory disease. In primary pulmonary hypertension, which may become manifest in childhood, fatigue, dyspnea, chest pain, and syncope are common symptoms. However, the disease process is generally well advanced before these symptoms become apparent. Auscultatory features of pulmonary hypertension include a pulmonary ejection sound, accentuation of the pulmonary component of the second heart sound, and the murmurs of pulmonary artery and tricuspid insufficiency. Although these features are mentioned in virtually every textbook on physical examination, there are very few studies that quantify their sensitivity or specificity in the detection of pulmonary hypertension. Attempts to quantify Reprint requests: Howard P. Gutgesell. MD. Department of Pediatrics. Box 386, University of Virginia Medical Center. Charlottesville, VA 22908.

auscuitatory findings by use of phonocardiography have produced only marginal improvement. For example, analysis of the components of the second heart sound in patients with atrial septal defect do not reliably distinguish those with Pulmonary hypertension. 1 Thus, although clues that suggest the presence of pulmonary hypertension may be obtained by history and physical examination, their specificity and sensitivity are largely undocumented (especially in infants and young Children). Moreover, fairly advanced degrees of pulmonary hypertension are often present when these findings become apparent. ELECTROCARDIOGRAPHY VECTORCARDIOGRAPHY

AND

Elevated pulmonary artery pressure results in right ventricular hypertrophy, which is ultimately detectable by electrocardiography. Despite the widespread use of elecPEP RVET

Preejectionperiod Right ventricular ejection time

trocardiography for many years, there are few studies that address sensitivity and specificity in detecting elevated pulmonary artery pressure in children. The greatest usefulness has been in evaluation of uncomplicated ventricular septal defect 2 and in detection of pulmonary hypertension in patients with chronic respiratory diseases such as cystic fibrosis. 3 In the evaluation of patients with ventricular septal defects, however, electrocardiography has the following limitations: (1) left ventricular hypertrophy may mask right ventricular hypertrophy and thus cause an underestimation of pulmonary artery pressure, and (2) coexistent pulmonary stenosis also produces right ventricular hypertrophy and will cause overestimation of pulmonary artery pressure. Likewise, the technique cannot be used to esti-

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disappearance of vectorcardiography from clinical use in most medical centers. ECHOCARDIOGRAPHY

RVET

"

>77"2

__._~ - ~ B

'~-~-'-..-z---

PEP/RvET=0)+5

Fig. t. Mimode echocardiographic recordings from normal child, A, and from patient with severe pulmonary hypertension, B. Note that in normal child, pulmonary valve leaflets gradually move posteriorly in diastole, with abrupt posterior dip (arrow) associated with atrial contraction. In the presence of pulmonary hypertension, valve leaflets remain immobile in diastole, with loss of atrial dip. PEP is prolonged and RVET shortened, resulting in elevated PEP/RVET ratio.

mate pulmonary artery pressure in patients with complex intracardiac lesions such as single ventricle or transposition of the great arteries. The electrocardiogram does not appear to be sufficiently sensitive in detecting mild degrees of pulmonary hypertension in patients with chronic respiratory disease. However, right ventricular hypertrophy, when present, is clearly associated with advanced pulmonary disease and elevated pulmonary artery pressure. Vectorcardiography has also been used in an attempt to estimate pulmonary artery pressure in patients with either ventricular septal defect or respiratory disease. Any additional accuracy obtained has been more than offset by the

Echocardiography is the most widely used noninvasive technique used to estimate pulmonary artery pressure. Three separate methods are available: M-mode, twodimensional, and Doppler. M-mode eehoeardiography. Early M-mode echocardiographic studies 4'5 demonstrated abnormalities in the pattern of pulmonary valve motion in patients with pulmonary hypertension. These included a loss of the normal posterior motion in diastole (reduced e-f slope), loss or diminution of the dip after atrial contraction, greater velocity of valve opening, and partial closure (notching) of the valve leaflets in mid systole (Fig. 1). Subsequent studies 6'7 suggested that these motion abnormalities are fairly specific but not sufficiently sensitive for the detection of pulmonary hypertension. Quantitative approaches to analysis of the M-mode eehocardiogram have attemRted to estimate pulmonary artery pressure by measurement of right ventricular systolic or diastolic time intervals. 8-12 Use of the systolic time interval is based on the Observation that as pulmonary artery pressure rises, the right ventricular preejection period lengthens, often with shortening of the right ventricular ejection time. The interval is often expressed as the P E P / R V E T ratio, which has a positive relationship to pulmonary artery pressure? Values greater than 0.30 suggest the possibility of elevated pulmonary artery pressure. and values greater than 0.40 are definitely abnormal. The clinical utility of the right ventricular systolic time intervals has been questioned. H Although virtually all investigators have found a direct relationship between the P E P / R V E T ratio and pulmonary artery pressure in crosssectional studies of large groups of patients, the scatter of the data is such that estimation of pulmonary artery pressure in an individual patient may be difficult. Limitations of the technique include (1) inability to obtain high-quality recordings of pulmonary valve motion in some patients, especially those with respiratory disease, and (2) the influence of variables such as heart rate, conduction disturbances, and myocardial contractility, which also affect the systolic time intervals. Some of these limitations can be overcome by measurement of right ventricular isovolumetric contraction time, the interval from the closure of the tricuspid valve to the opening of the pulmonary valve. A value greater than 25 msec suggests elevated pulmonary artery pressure. 13 Measurement of right ventricular diastolic time inter-

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Fig. 2. Two-dimensional echocardiogram in parasternal shortaxis projection from patient with suprasystemic right ventricular pressure, interventricular septum appears to be flat at end of diastole, and at end of systole, it has reversed its normal curvature to become convex toward left ventricle. (From King ME, Braun H, Goldblatt A, Liberthson R, Weyman AE. Circulation 1983;68:68-75. Used with permission of the American Heart Association, Inc.)

vals has also been applied to estimation of pulmonary artery pressure. In theory, in the presence of elevated pulmonary artery pressure, a longer period is required for right ventricular pressure to drop from its peak systolic level to that of the right atrium and thereby allow opening of the tricuspid valve. Pulmonary artery pressure is estimated from the length of the isovolumetric relaxation time)< ~5 It is time-consuming and technically difficult to obtain a high-quality M-mode echocardiogram suitable for qualitative analysis and measurement of systolic and diastolic time intervals, and it may be impossible in patients with hyperexpanded lungs, obesity, or chest deformities. However, next to Doppler echocardiography, this is probably the most accurate noninvasive method of estimating pulmonary artery pressure. Two-dimensional eehocardiography. In the presence of elevated right ventricular pressure, the interventricular septum shifts toward the left ventricle and appears flattened when observed by two-dimensional echocardiography (Fig. 2). The radius of curvature of the septum may be calculated, and a value more than twice normal is thought to be a sensitive marker of right ventricular systolic hypertension. 16There are insufficient data to determine the usefulness of this technique in detecting mild elevations of pulmonary artery pressure. However, pulmonary hyper-

Fig. 3. Doppler echocardiograms obtained from main pulmonary artery in normal child, A, and in patient with severe pulmonary hypertension, B. Note that in normal child, flow velocity curve is symmetric, whereas in the presence of pulmonary hypertension, curve is skewed toward left, with peak velocity in early systole and rapid decline in velocity in mid and late systole (arrow). tension should be considered if the septum appears flattened at the end of systole. Doppler echocardiography. Doppler echocardiography provides a profile of the pulmonary flow velocity pattern. In normal subjects the velocity pattern is fairly symmetric: =velOcity gradually increases in early systole, reaches its peak at mid systole, and decreases in late systole (Fig. 3). In patients with pulmonary hypertension, the flow pattern is distorted and peak velocity is reached early in systole, followed by an abrupt decline in flow velocity during the last two thirds of systole. Attempts ~ave been made to quantify this phenomenon by calculating the acceleration time (time from onset of flow to peak velocity) and

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Fig. 4. Doppler echocardiogram obtained from right atrial side of tricuspid valve. Systolic jet has peak velocity of 2.33 m/sec. This yields predicted "gradient" between right ventricle and right atrium of 22 mm Hg. Assuming normal right atrial pressure, peak right ventricular pressure is less than 30 mm Hg.

expressing it either in absolute terms or as a percentage of ejection time. 17,18 There is an inverse relationship between acceleration time and pulmonary artery pressure when the latter exceeds 50 mm Hg. We doubt the sensitivity of this technique for detection of early stages of pulmonary hypertension. In an animal study, ~9 we were unable to detect changes in the pulmonary artery flow pattern in dogs whose artery pressure was acutely increased nearly 100% by serotonin infusion. In addition, when an increase in the heart rate was induced by atrial pacing (without change in pulmonary pressure), a decrease in acceleration time occurred. The use of Doppler-derived pulmonary artery flow intervals to estimate pulmonary artery pressure has several similarities with the use of M-mode-derived right ventricular systolic time intervals. The measured intervals are influenced by numerous variables (heart rate, ventrieular function, and even the Doppler sampling site within the pulmonary artery) in addition to pulmonary artery pressure. There is a close correlation between the measured interval (or ratio of intervals) and pulmonary artery pressure in most studies, but the scatter of data limits usefulness except at the extremes of pressure. A second Doppler echocardiographic method for estimation of pulmonary artery pressure is based on the observation that the pressure gradient between two adjacent points in the cardiovascular system can be estimated with remarkable accuracy by the formula P = 4 V2, where P is the pressure difference (gradient) and V is the velocity of blood flow in meters per second. Doppler echocardiogra-

The Journal of Pediatrics May 1989

phy allows measurement of flow velocity. For estimation of pulmonary artery pressure by this technique, either tricuspid insufficiency, a ventricular septal defect, or a systemic artery-pulmonary artery connection is required. The Doppler echocardiogram is used, for example, to measure the velocity of the tricuspid regurgitant jet, which is present in a high proportion of patients with elevated pulmonary artery pressure. The velocity value is squared and multiplied by 4 to give the estimated systolic gradient between the right ventricle and the right atrium (Fig. 4). By adding an assumed or measured value for right atrial pressure, one can estimate the peak right ventricular systolic pressure. 2~ In the absence of pulmonary stenosis, this is also the pulmonary artery systolic pressure. Similar reasoning is used in the presence of a ventricular septal defectZ2-24; systemic artery (and thus left ventricular) systolic pressure is measured by sphygmomanometry. Doppler echocardiography is used to estimate the pressure gradient across the ventrieular septal defect. Subtraction of this gradient from left ventricular pressure provides an estimate of right ventricular pressure--and thus pulmonary artery pressure. In the presence of a patent ductus arteriosus or a systemic-pulmonary anastomosis, pulmonary artery systolic pressure is estimated by the velocity of the jet entering the pulmonary arteries from the systemic circulation. Chan et al. z5 recently compared three Doppler techniques for estimating pulmonary artery pressure in 50 patients undergoing cardiac catheterization. At least one of the methods could be employed in 96% of the patients. The authors concluded that the tricuspid gradient method (possible in 72% of patients) was the most useful and practical. Their data indicate that for a predicted pulmonary artery systolic pressure of 55 mm Hg, observed pressures ranged from 45 to 75 mm Hg. The Doppler-gradient method of estimating pulmonary artery pressure has an intrinsic appeal over most other methods in that it uses a measurement (blood flow velocity) that is a direct consequence of intracardiac or intravascular pressures. In the absence of left-to-right shunts, the method is applicable only to subjects with tricuspid insufficiency. In this setting, it is likely to be fairly specific for elevated right ventricular pressure. There are no known factors that spuriously elevate the flow velocity signal. However, the potential for underestimation of right ventricular pressure exists if the Doppler examination does not detect the flow jet of highest velocity. There is also a possibility of underestimating right ventricular peak systolic pressure when the interventricular gradient method is employed. The Doppler technique depicts peak, instantaneous pressure gradients. Because the rise in right ventricular pressure typically lags behind the rise in left ventric-

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ular pressure in early systole, a large estimated gradient at this time may not accurately reflect the ultimate systolic pressure in therright ventricle.

there does not appear to be a linear relationship between right ventricular wall thickness measured by thallium images and pulmonary artery pressure.

SUPPLEMENTARY

CORRELATION UTILITY

TECHNIQUES

Chest roentgenography and computed tomography. In the presence of pulmonary hypertension, the pulmonary arteries become enlarged and right ventricular dilation ultimately occurs. Because cardiac size and the diameter of portions of the pulmonary arterial tree can be estimated by the chest roentgenogram, and even more precisely by computed tomography, attempts have been made to quantify cardiac and pulmonary arterial size and to relate these variables to pulmonary artery pressure. 26,27 These studies have been largely limited to adults with mitral stenosis or primary pulmonary hypertension, conditions in which the volume of pulmonary artery flow is normal (or even reduced) and any increase in pulmonary artery diameter is probably a direct result of increased pressure. Less precise methods in heterogeneous groups of patients of various ages will undoubtedly be less accurate. Techniques such as computed tomography and magnetic resonance imaging may be of value as screening tests for pulmonary hypertension in selected pediatric groups (e.g., adolescents with cystic fibrosis); in whom,~ai'iables such as body size and volume of pulmonary artery flow are relatively constant. Radionucllde techniques. Two forms of radionuelide studies have been used to assess pulmonary artery (or right ventricular) pressure: radionuclide angiography for determination of right ventricular ejection fraction and thallium 201 myocardial perfusion images to determine right ventricular size and wall thickness. Right ventricular ejection fraction can be determined from either first-pass or gated equilibrium studies. Right ventricular ejection fraction is expressed as the difference in radioactivity counts between the end of diastole and the end of systole, divided by end-diastolic counts. Several studies in adults zs.29 demonstrate a negative relationship between right ventrieular ejection fraction and pulmonary artery pressure. Others, 3~ however, have found that the ejection fraction maintained near normal levels in patients with elevated pulmonary artery pressure. Conversely, false positive study results might be expected in patients with a decreased right ventricular ejection fraction caused by myocardial disease or coronary artery disease. The right ventricular free wall is normally not visualized (or is barely visualized) on thallium 201 myocardial perfusion images, but it becomes increasingly visible as the right ventricular diameter and free wall thickness increase)l.3z Clear-cut visualization of the right ventricle suggests right ventricular pressure or volume overload, but

VERSUS CLINICAL

In most of the studies cited, investigators attempted to relate one or more noninvasive measurements (right ventricular ejection fraction, P E P / R V E T ratio) to pulmonary artery pressure, often by linear regression analysis. In many instances, there is a reasonably strong correlation between the measured variable and pulmonary artery pressure when cross-sectional data from a large group of subjects are examined. This finding frequently leads to the suggestion that the noninvasive measurement is of clinical value in estimation of pulmonary artery pressure in individual patients, a claim that is not often supported by the data. CONCLUSIONS

AND RECOMMENDATIONS

It is obvious that the clinician cannot just "order an 'echo' to rule out pulmonary hypertension," as is occasionally overheard in the clinic and the intensive care unit. Noninvasive techniques with various costs, complexities, and degrees of accuracy are available to estimate pulmonary artery pressure. Appropriate use requires an understanding of accuracy and limitations, of the relative likelihood that the patient has pulmonary hypertension, and of the consequences of an inaccurate prediction. The following approach is suggested. In patients in whom the likelihood of elevated pulmonary artery pressure is relatively low (patients with clinical features of a small ventricular septal defect or uncomplicated asthma), screening by physical examination and an electrocardiogram is generally adequate. For patients at moderate risk (medium-sized ventricular septal defect with congestive heart failure, severe forms of left ventricular outflow obstruction, severe chronic respiratory disease), in addition to the physical examination and electrocardiogram a comprehensive echocardiographic evaluation is indicated. This should include M-mode echocardiography with measurement of right ventricular systolic time intervals, two-dimensional echocardiography for evaluation of septal curvature, and analysis of the Dopplerderived pulonary artery flow pattern and tricuspid insufficiency jet (if present). If these studies uniformly suggest low pulmonary artery pressure, further tests are unnecessary. If the results are discordant or suggest elevated pulmonary artery pressure, further tests are warranted. In patients with certain forms of congenital heart disease, cardiac catheterization and possibly surgical repair may be indicated. In patients with respiratory disease, electrocar-

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diographic and echocardiographic features of pulmonary hypertension confirm the severity of the underlying condition and indicate a need for intensive therapy. For high-risk patients (atrioventricular canal, transposition of the great arteries with ventrieular septal defect, persistent fetal circulation in the neonate), noninvasive evaluation using any techniques will demonstrate features of pulmonary hypertension. However, in those patients with congenital heart disease, direct measurement of pulmonary artery pressure and calculation of pulmonary resistance is generally necessary in planning the timing of surgical intervention. Thus patients with the extremes of pulmonary artery pressure (very low or very high) can be distinguished by history, physical examination, and electrocardiogram. Echocardiography is best used to confirm this impression and to help categorize certain patients with intermediate degrees of pulmonary hypertension. More expensive noninvasive investigation with computed tomography or radionuclide techniques does not appear to confer additional accuracy. Finally, refinements in cardiac catheterization techniques have reduced the risks and radiation exposure, and direct measurement of pulmonary artery pressure should be undertaken if the results of noninvasive testing are equivocal or if the consequences of an erroneous estimate of pulmonary artery pressure are great.

REFERENCES

1. Sutton G, Harris A, Leatham A. Second heart sound in pulmonary hypertension. Br Heart J 1968;30:743-56. 2. Witham AC, McDaniel JS. Electrocardiogram, vectorcardiogram, and hemodynamics in ventricular septal defect. Am Heart J 1970;79:335-46. 3. Siassi B, Moss A J, Dooley RR. Clinical recognition of cor pulmonale in cystic fibrosis. J PEDIATR 1977;78:794-5. 4. Weyman AE, Dillon JC, Feigenbaum H. Eehocardiographic patterns of pulmonic valve motion with pulmonary hypertension. Circulation 1974;50:905-10. 5. Nanda NC, Gramiak R, Robinson TI, Shah PM. Echocardiographic evaluation of pulmonary hypertension. Circulation 1974;50:575-81. 6. Marin-Garcia J, Mailer JH, Mirvis DM. The pulmonic valve echogram in the assessment of pulmonary hypertension in children. Pediatr Cardiol 1983;4:209-14. 7. Lew W, Karliner JS. Assessment of pulmonary valve echogram in normal subjects and patients with pulmonary arterial hypertension. Am Heart J 1979;42:147-61. 8. Hirschfeld S, Meyer R, Schwartz DC, Korfhagen J, Kaplan S. The echocardiographic assessment of pulmonary artery pressure and pulmonary vascular resistance. Circulation 1975;52:642-50. 9. Spooner EW, Perry BL, Stern AM, Sigmann JM. Estimation of pulmonary/systemic resistance ratios from echocardiographic systolic time intervals in young patients with congenital or acquired heart disease. Am J Cardiol 1978;42:810-6.

The Journal of Pediatrics May 1989

10. Gutgesell HP. Echocardiographie estimation of pulmonary artery pressure in transposition of the great arteries. Circulation 1978;57:1151-3. 11. Silverman NH, Snider AR, Rudolph AM. Evaluation of pulmonary hypertension by M-mode echocardiography in children with ventricular septal defect. Circulation 1980; 61:1125-32. 12. Oberhansli l, Branden G, Girod M, Friedli B. Estimation of pulmonary artery pressure by ultrasound: a study comparing simultaneously recorded pulmonary valve echogram and pulmonary arterial pressures. Pediatr Cardiol 1982;2:123-30. 13. Johnson GL, Meyer RA, Korfhagen J, Schwartz DC, Kaplan S. Echocardiographic assessment of pulmonary arterial pressure in children with complete right bundle branch block. Am J Cardiol 1978;41:1264-9. 14. Stevenson JG, Kawabori I, Guntheroth WG. Noninvasive estimation of peak pulmonary artery pressure by M-mode eehocardiography. J Am Coll Cardiol 1984;4:1021-7. 15. Bourlon F, Fouron JC, Battle-Diaz J, Ducharmee G, Davignon A. Relation between isovolumic relaxation period of the left ventricle and pulmonary artery pressure in d-transposition of the great arteries. Br Heart J 1980;43:226-31. 16. King ME, Braun H, Goldblatt A, Liberthson R, Weyman AE. Interventrieular septal configuration as a predictor of right ventricular systolic hypertension in children: a crosssectional echocardiographic study. Circulation 1983;68:6875. 17. Kosturakis D, Goldberg J, Allen HD, Loeber C. Doppler echocardiographic prediction of pulmonary arterial hypertension in congenital heart disease. Am J Cardiol 1984;53: 1110-5. 18. Martin-Duran R, Larman M, Trugeda A, et al. Comparison of Doppler-determined elevated pulmonary arterial pressure with pressured measured at cardiac catheterization. Am J Cardiol 1986;57:859-63. 19. Gutgesell HP, Kaul S, Oliner J, Kelly P. Influence of heart rate, pulmonary blood flow, and pulmonary artery pressure on the Doppler-derived pulmonary flow velocity pattern [Abstract]. Circulation 1986;74(II):II-381. 20. Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid incompetence. Circulation 1984;70:657-62. 21. Currie PJ, Seward JB, Chan KL, et al. Continuous-wave Doppler determination of right ventricular pressure: a simultaneous Doppler-catheterization study in 125 patients. J Am Coll Cardiol 1985;6:750-6. 22. Marx G, Allen H, Goldberg S. Doppler echocardiographic estimation of systolic pulmonary artery pressure in pediatric patients with interventricular communications. J Am Coll Cardiol 1985;6:1132-7. 23. Murphy DJ Jr, Ludomirsky A, Huhta JC. Continuous-wave Doppler in children with ventricular septal defect: noninvasive estimation of interventricular pressure gradient. Am J Cardiol 1986;57:428-32. 24. Silbert DR, Brunson SC, Schiff R, Diamont S. Determination of right ventricular pressure in the presence of a ventricular septal defect using continuous-wave Doppler ultrasound. J Am Coll Cardiol 1986;8:379-84. 25. Chan K-L, Currie P J, Seward JB, Hagler D J, Mair DD, Tajik J. Comparison of three Doppler ultrasound methods in the prediction of pulmonary artery pressure. J Am Coil Cardiol 1987;9:549-54.

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26. Lupi E, Dumont C, Tejada VM, Horwitz S, Galland F. A radiologic index of pulmonary arterial hypertension. Chest 1975;68:28-31. 27. Kuriyama K, Gamsu G, Stern R, Cann CE, Herfkens RJ, Brundage BH. CT-determined pulmonary artery diameters in predicting pulmonary hypertension. Invest Radioi 1984; 19:16-22. 28. Brent BN, Mahler D, Matthay RA, Berger H J, Zaret BL. Noninvasive diagnosis of pulmonary arterial hypertension in chronic obstructive pulmonary disease: right ventricular ejection fraction at rest. Am J Cardiol 1984;53:1349-53. 29. Brent BN, Berger HJ, Matthay RA, Mahler D, Pytuk L, Zaret BL. Physiologic correlates of right ventricular ejection fraction in chronic obstructive pulmonary disease: a combined

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radionuclide and hemodynamic study. Am J Cardiol 1982; 50:255-60. 30. Korr KS, Gandsman EJ, Winkler ML, Shulman RS, Bough EW. Hemodynamic correlates of right ventricular ejection fraction measured with gated radionuclide angiography. Am J Cardiol 1982;49:71-7. 31. Cohen HA, Baird MG, Rouleau JR, et al. Thallium 201 myocardiai imaging in patients with pulmonary hypertension. Circulation 1976;54:790-5. 32. Rabinovich M, Fisher KC, Treves C. Quantitative thallium201 myocardial imaging in assessing right ventricular pressure in patients with congenital heart defects. Br Heart J 1981;45:198-205.

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