Asian Cardiovasc Thorac Ann 2008;16:221-225
© 2008 Asia Publishing EXchange Ltd
Estimation of Pulmonary Vascular Resistance with Doppler Diastolic Gradients
Mehnaz Atiq, MD,
Habiba Tasneem, MD1,
Kalimuddin Aziz, FAAP1
Department of Pediatric Cardiology, The Aga Khan University Hospital
1 National Institute of Cardiovascular Diseases, Karachi, Pakistan
For reprint information contact: Mehnaz Atiq, MD, Tel: 92 21 493 0051 Ext. 4722, Fax: 92 21 493 4294, Email: mehnaz.atiq{at}aku.edu, Department of Pediatrics, The Aga Khan University Hospital, PO Box 3500, Karachi-74800, Pakistan.
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ABSTRACT
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This study was undertaken to determine the diastolic Doppler echocardiographic correlates of pulmonary vascular resistance calculated on cardiac catheterization in patients with secondary pulmonary arterial hypertension. Thirty-eight consecutive patients with congenital heart disease, pulmonary artery hypertension and pulmonary regurgitation were studied. Continuous-wave Doppler-derived pulmonary artery diastolic gradients were measured at 3 points on the pulmonary regurgitant diastolic velocity slope: peak diastolic, end-diastolic (at the R wave on the electrocardiogram), and mid-diastolic (midway between the peak and end-diastolic points). Catheterization data included oximetry, measurements of pressure in the cardiac chambers and great arteries, and calculation of pulmonary vascular resistance index. Doppler-derived peak, mid, and end-diastolic pulmonary regurgitation gradients correlated best with catheterization-measured pulmonary artery systolic, mean and diastolic pressures, respectively. The best Doppler correlate of pulmonary vascular resistance index was the pulmonary artery end-diastolic gradient. Clinically useful information can be obtained from Doppler pulmonary artery diastolic gradients measured on the pulmonary regurgitant diastolic velocity slope, which can estimate the pulmonary arterial pressure as well as pulmonary vascular resistance obtained on cardiac catheterization.
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INTRODUCTION
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Ventricular septal defect and other congenital cardiac anomalies causing increased pulmonary blood flow leading to pulmonary artery hypertension (PAH) and obstructive pulmonary vascular disease.1 In Asia, a large number of patients with uncorrected congenital cardiac anomalies are referred late.2 Most are found to have PAH and pulmonary vascular disease on cardiac catheterization. Assessment of the degree of PAH and the hemodynamic status of the pulmonary vasculature is a major component of treatment evaluation, but how best to do this is still debated. The aim of cardiac catheterization in such situations is to measure pulmonary artery (PA) pressures, pulmonary blood flow and pulmonary vascular resistance. Current methods to evaluate PAH and vascular reactivity through measurement of pulmonary vascular resistance, which is the ratio of mean pressure drop across the pulmonary vasculature to mean pulmonary flow, are based on the assumption of steady hemodynamics.3 Pulmonary artery pressure is routinely estimated by Doppler echocardiography using the velocity of tricuspid regurgitation.1,4 When right ventricular outflow tract obstruction is absent, the Doppler peak systolic gradient of tricuspid regurgitation indicates PA systolic pressure.5–7 In adults without an intracardiac shunt, Doppler estimation of PA diastolic pressure has been made by measuring the end-diastolic gradient of the pulmonary regurgitation velocity and adding it to the clinical estimate of right atrial pressure.8 It would be helpful if patients with secondary PAH who have pulmonary vascular disease could be differentiated by Doppler echocardiography. The objective of this study was to find a correlation between PA pressure and the calculated pulmonary vascular resistance index (PVRI) obtained by cardiac catheterization and the Doppler-derived PA diastolic gradients.
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PATIENTS AND METHODS
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This prospective study enrolled 38 consecutive children with a congenital heart disease and PAH who had pulmonary regurgitation on echocardiography. A detailed history, clinical examination, chest radiography, 12-lead electrocardiogram, 2-dimendional echocardiography, color-flow mapping and spectral Doppler studies were obtained for each patient on entry into the study. There were 21 (55%) males. Ages ranged from 3 months to 15 years, with a mean of 5.1 ± 3.7 years. The diagnoses included isolated ventricular septal defect in 23 children, double-outlet right ventricle in 4, ventricular and atrial septal defects in 4, ventricular septal defect and patent ductus arteriosus in 3, and one each of patent ductus arteriosus with atrial septal defect and mitral regurgitation, atrial septal defect and patent ductus arteriosus and single ventricle with malposed great vessels. Cardiac catheterization was undertaken to measure PA pressures and PVRI. Doppler studies were repeated in all patients after cardiac catheterization. The team performing the echocardiography was blinded to the cardiac catheterization data.
Doppler studies were performed using Sonos 5500 echocardiography equipment (Philips Medical Systems, Andover, MA, USA) with 5-MHz and 3.75-MHz transducers for younger and older children, respectively. Doppler measurements were obtained in continuous-wave Doppler mode with a simultaneous lead II electrocardiogram displayed on the monitor. During the first study, patients were awake (except toddlers who were sedated with chloral hydrate 50 mg · kg–1). The 2-dimendional, color-flow mapping and Doppler examinations were carried out, and the pulmonary regurgitation flow was identified on color-flow mapping with the transducer in the parasternal short-axis position. The Doppler beam was aligned with the flow of the regurgitant jet so that maximum Doppler frequency shifts could be obtained on audio signals, and a complete envelope of the pulmonary regurgitation slope could be seen on the screen. The slope was characterized by a peak velocity soon after closure of the pulmonary valve, and a slow deceleration slope thereafter until the pulmonary valve reopened. Measurements were taken at 3 different points on this regurgitant diastolic velocity slope: peak diastolic velocity; end-diastolic velocity occurring at the time of the R wave on the electrocardiogram; and a mid-diastolic velocity point, midway between the peak and end-diastolic velocity points (Figure 1
). An average of at least 4 measurements was used for quantitative analysis. The gradient between the PA and the right ventricle was calculated using the modified Bernoulli equation: the pressure gradient was 4 x V2, where V is the velocity in meters per second. The regurgitant volume or fractions were not calculated.
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Figure 1. Doppler measurement of diastolic gradients on the slope pulmonary regurgitation envelope; the end-diastolic gradient was at the R wave on the electrocardiogram, peak diastolic was after the T wave, and the mid-diastolic gradient was between the two.
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For cardiac catheterization, all patients were sedated with intravenous pethidine hydrochloride 2.5 mg · kg–1, chlorpromazine 0.5 mg · kg–1 and promethazine 0.5 mg · kg–1. Pressures were recorded with fluid-filled catheters, and oximetry was carried out in the standard manner. The systolic, mean and diastolic pressures were measured from PA pressure tracings. The diastolic PA pressure was measured at the time of the R wave on the electrocardiogram during expiration. Right ventricular systolic and end-diastolic pressures were recorded, and left atrial or pulmonary capillary wedge pressures were determined. Pulmonary and systemic blood flow (L · min–1) and vascular resistance (Wood units) were calculated using an assumed value of oxygen consumption, according to the derived oxygen consumption by LaFarge and Miettinen.9 Pulmonary vascular resistance index was calculated by dividing pulmonary vascular resistance by body surface area.
Data were analyzed using SPSS version 13 (SPSS, Inc., Chicago, IL, USA) and Epi Info version 6 (Centers for Disease Control and Prevention, Atlanta, GA, USA) software. Analysis of variance was used to compare pressures and gradients between groups. Correlation between pressures measured by Doppler and the cardiac catheterization data was carried out by multivariate analysis and analysis of regression coefficient.
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RESULTS
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A significant correlation was found between the Doppler-derived pressure gradients of the pulmonary regurgitant velocity spectrum and the systolic, mean, and diastolic PA pressures on catheterization. The Doppler peak pressure gradient of the pulmonary regurgitation slope correlated best with the systolic PA pressure from catheterization (r = 0.84, p < 0.0001). The Doppler midpoint pressure gradient correlated with the mean PA pressure (r = 0.88, p < 0.0001). The Doppler-derived gradient at the end-diastolic point correlated significantly with the catheterization-derived PA diastolic pressure (r = 0.86, p < 0.0001; Figure 2). The catheter PA diastolic pressure was converted to the pressure gradient at the right ventricular outflow tract by subtracting the right ventricular end-diastolic pressure, and these measurements were compared with the Doppler end-diastolic pressure gradient. This also showed a highly significant linear correlation (r = 0.83, p < 0.0001, Table 1). Pulmonary vascular resistance index was found to correlate best with the catheter PA end-diastolic pressure (r = 0.79, p < 0.0001, Figure 3) compared to mean and systolic pressures (r = 0.73 and r = 0.71, respectively; Table 1). Pulmonary vascular resistance index was also linearly best related to the Doppler PA end-diastolic pressure gradient (r = 0.92, p < 0.000l; Figure 4). The regression equation to estimate PVRI from the Doppler PA end-diastolic pressure gradient (in mm Hg) was calculated as: PVRI = –8.91 + 0.53 x PA end-diastolic pressure gradient.
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Figure 2. Correlation of pulmonary artery (PA) end-diastolic pressure on catheterization and on Doppler echocardiography (r = 0.86, r2 = 0.77, y = 2.128, p < 0.0001).
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Figure 3. Correlation of pulmonary vascular resistance index (PVRI) and pulmonary artery (PA) end-diastolic pressure on catheterization (r = 0.79, r2 = 0.69, y = 27.147, p < 0.0001).
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Figure 4. Correlation of pulmonary vascular resistance index (PVRI) and Doppler pulmonary artery end-diastolic gradient (r = 0.92, r2 = 0.84, y = 19.049, p < 0.001).
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The 38 patients with PAH were separated into 3 groups according to PVRI (Table 2). The PA pressures (systolic, mean and end-diastolic) were inversely related to the pulmonary-to-systemic flow ratio of patients in groups 1, 2, and 3. Compared to group 1, PA end-diastolic pressures on catheterization were significantly higher in groups 2 and 3 ( p = 0.04, p = 0.0003, respectively) so that the higher the PVRI, the higher the PA end-diastolic pressure. Since the best correlate of PVRI was with catheter PA end-diastolic pressure and Doppler end-diastolic gradient, a Doppler end-diastolic gradient > 41.7 ± 7.4 mm Hg indicated severe PAH and PVRI > 8 Wood units · m–2.
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DISCUSSION
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The application of Doppler echocardiography to quantify PAH noninvasively is well recognized. A number of studies have addressed its use as a screening tool.1–11 The jet of tricuspid regurgitation has been analyzed in adults and children with PAH (primary or secondary) and significant correlations with right heart catheterization values were found.6,11 Doppler echocardiography was used to estimate PA diastolic pressure by others who found a good correlation with invasive measurements.8,10 However, no study has correlated it to PVRI. Our data confirm previous reports that Doppler velocities can be used to estimate PA pressures.5,12–17 Rudolph18 found PA diastolic pressure to be a valuable guide to PVRI in the presence of a large communication between the 2 ventricles. Our study also shows that the diastolic slope of the pulmonary regurgitant velocity on Doppler can be used to estimate PVRI, and that PA diastolic pressure measured by cardiac catheterization correlates best with PVRI. The Doppler-derived end-diastolic pressure gradient correlates with both diastolic pressure and PVRI calculated on catheterization.
Masuyama and colleagues13 showed that the Doppler peak gradient of the pulmonary regurgitant diastolic velocity slope correlated with catheterization-derived mean PA pressure, while our study showed that although Doppler peak velocity gradient correlated with mean PA pressure, the best correlation was with systolic PA pressure. This difference could be due to the patient population studied by Masuyama and colleagues,13 which included normotensive patients as well as those with mild and severe PAH, while all our patients had significantly elevated PA pressure and the majority (27/38, 70%) had high PVRI (> 3 Wood units · m–2). This also explains the much flatter diastolic slope of the pulmonary regurgitation envelope (Figure 1
), and the smaller difference between the peak, mean and end-diastolic gradients. Therefore, our study indicates that in patients with moderate to severely increased PA pressure, perhaps due to altered arterial input impedance and compliance, the end-diastolic Doppler gradient has a better correlation than that seen with the much steeper slope of mildly elevated PA pressure. A similar observation has been made by others.16–20 Another finding was that in the presence of a large shunt with equal systolic pressures in the PA and aorta, PA diastolic pressure may be a meaningful guide to PVRI in that if the diastolic pressure is 2/3 systemic, then the PVRI is high. If it is 1/3 to 1/2, then PVRI is moderately raised.18
Our data also shows a significant linear correlation between Doppler- and catheterization-derived end-diastolic gradient in the PA (Figure 1). A similar observation was reported by Ge and colleagues14 in patients with patent ductus arteriosus, and also by Lee and colleagues8 in adult patients in a medical intensive care unit, where a good correlation was found between end-diastolic pulmonary gradient on cardiac catheterization and the Doppler-derived gradient corrected by adding the clinical estimate of right atrial pressure. Thus it seems reasonable to consider the Doppler-derived gradient to be a close approximation of the actual PA pressure for clinical reference.
In this study, PVRI was found to be related to catheterization-measured systolic and mean PA pressures (because all these variables measure pulmonary pressures), but best related linearly to end-diastolic pulmonary gradient, a finding that endorses previous observations made in our hospital and by others.2,18 We also established a strong relationship between Doppler end-diastolic pulmonary gradient and PVRI, which was highly significant ( p < 0.0001). Although limited by a sample size of 38 patients, this study included some with PAH, increased pulmonary blood flow and normal PVRI (group 1 on Table 2). This group could be clearly distinguished from those with PAH and increased PVRI. The relationship of PVRI with end-diastolic pulmonary gradient on catheterization as well as on Doppler studies showed significant differences between group 1 (normal PVRI), group 2 (moderately elevated PVRI), and group 3 with PVRI > 8 Wood units · m–2. It therefore seems that the Doppler-derived end-diastolic pulmonary gradient is an important parameter in the estimation of PVRI. For clinical purposes, the Doppler-derived end-diastolic pulmonary gradient can be used for patient selection for urgent cardiac catheterization and also for follow-up of patients to assess the response to drugs used in severe PAH. The Doppler end-diastolic pulmonary gradient at which one would expect a high PVRI would be 41.7 ± 7.4 mm Hg (Table 2), or we could apply the derived regression equation (see Results). One of the few limitations of the methodology is the difficulty in obtaining a good envelope of pulmonary regurgitation on Doppler echocardiography. The presence of right ventricular dysfunction with elevated end-diastolic pressures would introduce an error in the estimation of PVRI based on Doppler end-diastolic gradients. It was concluded that Doppler pulmonary diastolic gradients reflect PA pressures in patients with PAH. The Doppler pulmonary end-diastolic gradient correlates with PVRI and can be used to separate patients with a normal PVRI from those with a high PVRI.
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ACKNOWLEDGMENTS
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We would like to acknowledge the statistical help provided by Mr Iqbal Azam, Department of Community Health Sciences, Section of Medical Statistics, Aga Khan University Hospital, Karachi.
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ABSTRACT
INTRODUCTION
