Systemic vascular resistance (SVR) is an integral

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1 Noninvasive Measurement of Systemic Vascular Resistance Using Doppler Echocardiography Amr E. Abbas, MD, F. David Fortuin, MD, FACC, Bhavesh Patel, MD, Carlos A. Moreno, BS, Nelson B. Schiller, MD, FACC, and Steven J. Lester, MD, FACC, Royal Oak, Michigan; Scottsdale, Arizona; and San Francisco, California Background: Systemic vascular resistance (SVR) is an integral therapeutic component of patients with heart failure and shock. We hypothesized that the ratio of the peak mitral regurgitant velocity (MRV) (m/s) to left ventricular outflow time-velocity integral (TVI LVOT ) (cm) by Doppler would provide a noninvasive correlate of SVR. Methods: SVR was correlated to MRV/TVI LVOT in 33 patients undergoing right heart catheterization. Receiver operating characteristic curves were generated to determine the best-balanced sensitivity and specificity to identify SVR > 14 Wood units (WU) and <10 WU. Results: MRV/TVI LVOT correlated well with SVR (r 0.842, 95% confidence interval , P <.001, Y *X). By receiver operating characteristics, MRV/TVI LVOT > 0.27 had a 70% sensitivity and a 77% specificity to identify SVR > 14 WU. MRV/TVI LVOT < 0.2 had a 92% sensitivity and a 88% specificity to identify SVR < 10 WU. Conclusion: Doppler echocardiography provides a reliable noninvasive assessment of SVR. (J Am Soc Echocardiogr 2004;17:834-8.) Systemic vascular resistance (SVR) is an integral component of arterial blood pressure determination used to monitor the treatment of patients who are critically ill with congestive heart failure and shock. Evaluation of SVR becomes essential for patients with shock to help identify the cause of ineffective tissue perfusion resulting in cellular dysfunction. To date, the only accepted method for the determination of SVR is by invasive hemodynamic measures. SVR is calculated by the ratio of transsystemic pressure gradient to transsystemic flow. 1 Normal SVR values range from 10 to 14 Wood units (WU). Doppler echocardiography has significantly impacted clinical medicine by its ability to noninvasively determine intracardiac hemodynamics including pressure and flow. 2-9 Because flow and pressure variables can be determined, we hypothesized that a measure of SVR could be accurately derived by Doppler echocardiography. From William Beaumont Hospital, Royal Oak, Michigan (A.E.A.); Mayo Clinic Scottsdale; and University of California, San Francisco (N.B.S.). Reprint requests: Amr E. Abbas, MD, Division of Cardiovascular Diseases, William Beaumont Hospital, 3601 W 13 Mile Rd, Royal Oak, MI ( aabbas@beaumont.edu) /$30.00 Copyright 2004 by the American Society of Echocardiography. doi: /j.echo METHODS This study was approved by our institutional review board. A convenience sample of 41 patients who had a pulmonary artery catheter in place was evaluated. Written informed consent was obtained from patients or the next of kin if patients were unable to provide consent. Doppler and invasive measurements were obtained within 45 minutes of each other. A total of 8 patients met the exclusion criteria: no Doppler evidence of mitral regurgitation (3); severe tricuspid regurgitation (as determined by 2-dimensional, color Doppler, and spectral Doppler evaluation of the tricuspid inflow and hepatic venous flow) (2); aortic stenosis (mean gradient 20 mm Hg) (2); or mitral stenosis (1). SVR measurements were obtained invasively in Wood units. Invasive Measurements All patients were studied in the fasting state. A 7F Swan- Ganz catheter was used to obtain right atrial (RA) pressure (RAP). For patients in the catheter laboratory (n 23), an angulated pigtail catheter was placed in the ascending aorta to measure mean aortic pressure (MAP). Mean arterial pressure was measured invasively through a radial arterial line for patients located in the intensive care department (n 10). Cardiac output (CO) was calculated using the thermodilution method as a mean of 3 consecutive measurements not varying by more than 10%. This method was selected to standardize the measurements of CO between the cardiac catheterization laboratory and 834

2 Volume 17 Number 8 Abbas et al 835 Figure 1 Doppler tracings showing mitral regurgitant velocity (MRV) (left) and left ventricular outflow time-velocity integral (LVOT TVI) (right) in patient with increased ( 14 Wood units [WU]) systemic vascular resistance (SVR). MRV is 5.3 m/s and LVOT TVI is 15 cm. MRV/TVI LVOT ratio is 5.3/ ( 0.27, cutoff for elevated SVR). Patient s invasive SVR was 18 WU. Figure 2 Doppler tracings showing mitral regurgitant velocity (MRV) (left) and left ventricular outflow time-velocity integral (LVOT)(right) for patient with normal systemic vascular resistance (SVR). MRV is 5.3 m/s and LVOT is 22 cm. MRV/TVI LVOT ratio is 5.3/ ( 0.27, cutoff for elevated SVR). Patient s invasive SVR was 14 Wood units. the intensive care department. SVR, expressed in Wood units, was then calculated using the equation: SVR MAP RAP/CO. Doppler Measurements A cardiac ultrasound machine (Acuson Sequoia, Acuson, Mountainview, Calif) was used to obtain Doppler parameters. All images were digitally recorded on the hard drive and then stored on a removable disk. The left ventricular (LV) outflow time-velocity integral (TVI LVOT ) in centimeters was obtained by placing a pulsed wave sample volume in the LV outflow tract when imaged from the apical 3-chamber view. The sample volume was placed so that the closing, but not opening, click of the aortic valve was visualized. Continuous wave Doppler was used to determine peak mitral regurgitant velocity (MRV) in m/s. The highest velocity obtained from multiple echocardiographic views was used. If either spectral Doppler signal was suboptimal, injectable suspension of octafluoropropane (Definity, Bristol-Myers Squibb, New York, NY) was used to enhance the signal. For patients with atrial fibrillation or atrial flutter (n 9) the average of 5 measurements were used. The ratio MRV/TVI LVOT was then calculated (Figures 1 and 2). Both the individuals obtaining the invasive measurements and those obtaining the Doppler variables were blinded to each other s calculations. Statistical Analysis Software (SAS, Version 8, SAS Institute, Cary, NC) was used for statistical computations. Linear regression analysis was generated between SVR and MRV/TVI LVOT. The Pearson correlation coefficient and 95% confidence

3 836 Abbas et al August 2004 Table 1 Patient demographics, ejection fraction, and referral diagnosis Characteristic Findings Sex (M/F) 23/10 Mean age (y) 67 (45 83) Mean ejection fraction (range) 49% (15% 70%) Referral diagnosis CAD and exertional dyspnea 10 Valvular heart disease 6 Severe cardiomyopathy 5 Renal failure/renal transplant 4 evaluation End-stage liver disease/liver transplant 3 evaluation Acute respiratory failure 3 Pulmonary hypertension 3 Septic shock 2 Chest pain and exertional dyspnea 2 Severe GI bleeding 1 Intracranial hemorrhage 1 Postoperative 1 CAD, Coronary artery disease; F, female; GI, gastrointestinal; M, male. The sum of referral diagnosis is greater than the total number of patients because many patients had more than one diagnosis. Table 2 Hemodynamic characteristics of the patients Characteristic Findings MAP Mean (range) mm Hg 82 (41 121) MAP 65 mm Hg, n (%) 7 (21) RAP Mean (range) mm Hg 8 (1 27) RAP 8 mm Hg, n (%) 14 (42) PCWP Mean (range) mm Hg 15 (2 30) PCWP 18 mm Hg, n (%) 10 (30) CO Mean (range) L/min 6 ( ) CO 4 L/min, n (%) 4 (12) CO 6 L/min, n (%) 13 (39) SVR Mean (range) (WU) ( ) SVR 10 WU, n (%) 8 (24) SVR 14 WU, n (%) 14 (42) MRV/TVI LVOT Mean (range) 0.27 ( ) CO, Cardiac output; MAP, mean arterial pressure; MRV, peak mitral regurgitant velocity; PCWP, pulmonary capillary wedge pressure; RAP, right atrial pressure; SVR, systemic vascular resistance; TV LVOT, left ventricular outflow tract time-velocity integral; WU, Wood units. interval (CI) for the correlation were obtained. Two receiver operating characteristic curves were generated to determine SVR values with the best-balanced sensitivity and specificity to identify SVR 14 WU and 10 WU. A total of 25% of the Doppler images were re-evaluated to determine the intraobserver and interobserver reliability. Interobserver and intraobserver reliability for both MRV and TVI LVOT were quantified by calculating the intraclass correlation coefficient (ICC) ( 2 patients/( 2 patients 2 error). CI for the ICC were calculated by using the method of Shrout and Fleiss. 10 RESULTS Patient demographics, clinical characteristics, and referral diagnoses are shown in Table 1. In all, 10 patients were located in the intensive care department on hemodynamic support, 5 of whom were mechanically ventilated, and 7 with MAP 65 mm Hg. Complete hemodynamic findings of our patients are shown in Table 2. MRV/TVI LVOT correlated well with invasive SVR measurements (r 0.84, 95% CI , P.001, Y *X) (Figure 3). Using receiver operating characteristic analysis, MRV/TVI LVOT ratio of 0.27 had a sensitivity of 70% and a specificity of 77% to identify SVR 14 WU (area under the curve: 0.87). MRV/TVI LVOT ratio of 0.20 had a sensitivity of 92% and a specificity of 88% to identify SVR 10 WU (area under the curve: Figure 3 Linear regression analysis showing good correlation between systemic vascular resistance (SVR) in Wood units and mitral regurgitant velocity (MRV)/left ventricular outflow time-velocity integral (TVI LVOT )(r 0.842, 95% confidence interval , P.001, Y *X). 0.93) (Figure 4). Thus, this method has more sensitivity and specificity to identify patients with low versus high SVR. The ICC and CI for interobserver reliabilities for MRV were 0.98 (95% CI ) and for TVI LVOT were 0.94 (95% CI ). The ICC and CI for intraobserver reliabilities for MRV were 0.99 (95% CI ) and for TVI LVOT were 0.97 (95% CI ).

4 Volume 17 Number 8 Abbas et al 837 Figure 4 Receiver operating characteristic curves used to calculate mitral regurgitant velocity (MRV)/left ventricular outflow time-velocity integral (TVI LVOT ) with best-balanced sensitivity and specificity to determine elevated systemic vascular resistance (SVR)( 14 Wood units [WU]) (left) and low SVR ( 10 WU) (right). MRV/TVI LVOT 0.27 had sensitivity of 70% and specificity of 77% to identify SVR 14 WU, whereas ratio 0.2 had sensitivity of 92% and specificity of 87.5% to identify patients with SVR 10 WU. AUC, Area under the curve. DISCUSSION SVR is calculated by the ratio of transsystemic pressure gradient to transystemic flow. Together with CO, it determines mean arterial blood pressure. 1 Several neural and humoral factors influence the arteriolar tone, which is the major contribution to SVR. Shock is a state of tissue underperfusion that, if not corrected, manifests as hypotension, impaired cellular function, and finally cellular death and multiorgan failure. In patients who present with congestive heart failure or shock, a complex pathophysiologic process involving multiple neurohormonal pathways determines the SVR and the CO and, thus, blood pressure. SVR is low for patients with distributive type of shock (eg, septic shock), whereas it is increased for patients with hypovolemic, obstructive, and cardiogenic shock. 1 Thus, in association with clinical data, knowledge of SVR helps guide therapy and determine if patients require volume repletion, cardiotropic agents, or vasoactive agents. Traditionally, this has been performed by invasive right heart catheterization with its inherent potential complications and logistic limitations. A readily available, accurate, and noninvasive technique would be a valuable tool in the treatment of these patients. Transthoracic echocardiography can provide an accurate assessment of cardiac function. Moreover, Doppler echocardiography can determine intracardiac flow velocities and, therefore, be used to derive intracardiac pressures using the modified Bernoulli equation. It has been shown to provide accurate measures of RAP, 6 pulmonary pressures, 4,9 and LV filling pressure. 11 More recently we have shown it to be a valuable tool in estimating pulmonary vascular resistance. 12 In this study we propose a noninvasive method using Doppler echocardiography to assess SVR. There was a positive correlation between invasive SVR measurements and the ratio MRV/TVI LVOT. With progressive increase in SVR there was a corresponding increased in MRV/TVI LVOT. This correlation was derived from the following equations. According to the law of conservation of energy, potential energy is equal to kinetic energy. Thus: m * g * h 1/2 mv 2, where m is mass, g is gravitational constant, h is height, and v is velocity. Because m, g, 1/2, and exponential power are constants, the equation may be reduced to: h v (where means proportionate), because h is P, where P is pressure gradient. Thus: P v, because P is Q * R, where Q is flow and R is resistance. Thus:Q*R v. Rearranging the equation yields: R v/q. Calculating CO by Doppler, Q TVI LVOT * Area L - VOT * heart rate, where Area LVOT is the cross-sectional area of the LV outflow tract. Assuming unchanged area during the cardiac cycle and no wide variations in heart rate: R v/tvi LVOT,wherevis velocity across the systemic circulation. A negligible difference exists in absolute pressure measurements between the RA and left atrium compared with MAP. Thus, in this study we used MRV, which is the velocity of blood flow from the LV into the left atrium as a correlate of transystemic velocity of flow, which is the velocity of blood flow from LV into the systemic circulation and finally into the RA. Thus: SVR MRV/TVI LVOT. Study Limitations As with all Doppler echocardiographic measurements, proper alignment of the ultrasound beam to

5 838 Abbas et al August 2004 the regurgitant flow is crucial to ensure that the maximum MRV is determined. Determination of interobserver reliability was not performed at the bedside. However, there was good interobserver and intraobserver observer agreement for the recorded Doppler variables. Our method relies on a determination of MRV. MRV could be obtained in all but 3 patients. Previous reports have described a lesser prevalence of physiologic mitral regurgitation on Doppler echocardiography. 13 The use of manufactured ultrasound contrast agents can also be used to enhance the spectral Doppler signal when difficult to obtain and, hence, increase the external validity of this study. 14 Possible confounding variables that were not included in our Doppler equation include correlates of RAP, pulmonary capillary wedge pressure, and heart rate. However, our patient population spanned various degrees of these measurements (Table 2) and our correlation remained robust. We believe that this method should be applied in the context of the clinical picture and other noninvasive echocardiography and Doppler parameters and not be the sole determinant of management. Finally, patients in whom structural changes may influence the MRV (aortic and mitral stenosis) and invasive CO measure by thermodilution (severe tricuspid regurgitation) were excluded. Further studies will be needed to test this formula in this subset of patients. Conclusions Doppler echocardiography may provide a noninvasive assessment of SVR by using the formula MRV/ TVI LVOT. By providing noninvasive correlates of intracardiac pressure and flow, Doppler echocardiography may offer a complete hemodynamic assessment to help guide diagnosis and treatment of patients who are critically ill. Further evaluation of the prognostic implication of this ratio needs to be studied. The authors wish to acknowledge the echocardiography department at Mayo Clinic Scottsdale and Jose Hernandez, biostatistics department, for immense help in preparing this manuscript. REFERENCES 1. Parrillo J. Approach to the patient with shock. In: Goldman L, editor. Cecil textbook of medicine. 21st ed. Philadelphia: WB Saunders; p Berger M, Haimowitz A, Van Tosh A, Berdoff RL, Goldberg E. Quantitative assessment of pulmonary hypertension in patients with tricuspid regurgitation using continuous wave Doppler ultrasound. J Am Coll Cardiol 1985;6: Ge Z, Zhang Y, Ji X, Fan D, Duran CM. Pulmonary artery diastolic pressure: a simultaneous Doppler echocardiography and catheterization study. Clin Cardiol 1992;15: Hatle L, Angelsen BA, Tromsdal A. Non-invasive estimation of pulmonary artery systolic pressure with Doppler ultrasound. Br Heart J 1981;45: Ihlen H, Amlie JP, Dale J, Forfang K, Nitter-Hauge S, Otterstad JE, et al. Determination of cardiac output by Doppler echocardiography. Br Heart J 1984;51: Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol 1990;66: Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. Echocardiographic determination of mean pulmonary artery pressure. Am J Cardiol 2003;92: Masuyama T, Kodama K, Kitabatake A, Sato H, Nanto S, Inoue M. Continuous-wave Doppler echocardiographic detection of pulmonary regurgitation and its application to noninvasive estimation of pulmonary artery pressure. Circulation 1986;74: Yock PG, Popp RL. Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 1984;70: Shrout PEFJ. Intraclass correlations: uses in assessing rater reliability. Psychol Bull 1979;86: Ommen SR, Nishimura RA, Appleton CP, Miller FA, Oh JK, Redfield MM, et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: a comparative simultaneous Doppler-catheterization study. Circulation 2000;102: Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol 2003;41: Jobic Y, Slama M, Tribouilloy C, Lan Cheong Wal L, Choquet D, Boschat J, et al. Doppler echocardiographic evaluation of valve regurgitation in healthy volunteers. Br Heart J 1993;69: Dini FL, Traversi E, Franchini M, Micheli G, Cobelli F, Pozzoli M. Contrast-enhanced Doppler hemodynamics for noninvasive assessment of patients with chronic heart failure and left ventricular systolic dysfunction. J Am Soc Echocardiogr 2003;16: