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First published online on May 15, 2007
Chest, doi:10.1378/chest.06-2690
doi:10.1378/chest.06-2690
(Chest. 2007; 132:37-43)
© 2007 American College of Chest Physicians
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Right Ventricular Pressure Waveform and Wave Reflection Analysis in Patients With Pulmonary Arterial Hypertension*

Mustafa Karamanoglu, PhD; Michael McGoon, MD, FCCP; Robert P. Frantz, MD; Raymond L. Benza, MD; Robert C. Bourge, MD; Robyn J. Barst, MD, FCCP; Barbro Kjellström, BS and Tom D. Bennett, PhD

* From NT&D Research, Medtronic Inc. (Drs. Karamanoglu and Bennett, and Ms. Kjellström), Minneapolis, MN; Division of Cardiovascular Diseases (Drs. McGoon and Frantz), Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, MN; Department of Medicine (Drs. Benza and Bourge), University of Alabama at Birmingham, Birmingham, AL; and Department of Pediatrics (Dr. Barst), Columbia University College of Physicians and Surgeons, New York, NY.

Correspondence to: Mustafa Karamanoglu, PhD, NT & D Research, Medtronic Inc, 7000 Central Ave NE, CW320, Fridley, MN 55432; e-mail: mustafa.karamanoglu{at}Medtronic.com

Abstract

Background: Cardiac index is an important determinant of outcome in patients with idiopathic pulmonary artery hypertension (IPAH). An implantable hemodynamic monitor (IHM) [Chronicle; Medtronic; Minneapolis, MN; a system limited to investigational use only] that records right ventricular (RV) pressure waveforms continuously may increase our understanding of IPAH and improve therapeutic selections and outcomes. The aim of this study was to investigate whether the RV pressure waveform utilizing an IHM can be used to estimate the magnitude of pressure wave reflection and cardiac index in patients with IPAH in acute settings.

Methods: In eight patients with pulmonary arterial hypertension, RV pressure waveforms were recorded utilizing the IHM, and breath-by-breath cardiac index was recorded during acute IV epoprostenol infusion at 3, 6 and 9 ng/kg/min. Late systolic pressure augmentation and cardiac index were estimated using the RV pressure waveforms and correlated with direct measurement of cardiac index.

Results: At baseline, the cardiac index was 2.1 ± 0.2 L/min/m2, total pulmonary resistance index was 38 ± 2 Wood U/m2, and RV systolic pressure was 92 ± 4 mm Hg. Wave reflection accounted for 29 ± 1 mm Hg of the RV systolic pressure. During epoprostenol infusion, total pulmonary resistance index and wave reflection decreased (– 15 ± 4 Wood U/m2, p < 0.001, and – 5 ± 2 mm Hg, p < 0.05, respectively). The breath-by-breath cardiac index correlated with the RV pressure waveform cardiac index estimates (r2 = 0.95).

Conclusions: RV pressure waveform analysis provides continuous hemodynamic assessments including cardiac index in acute settings. Once confirmed in long-term settings, this information may prove useful in optimizing a treatment regimen in patients with IPAH.

Key Words: cardiac output • epoprostenol • pulmonary arterial hypertension • right ventricular pressure • wave reflection

Although idiopathic pulmonary arterial hypertension (IPAH), previously termed primary pulmonary hypertension, is a rare disease (ie, incidence of 2 to 3 persons per million per year), its morbidity and mortality remain high. Over the past decade, the therapeutic options for these patients have increased; however, decisions regarding how to optimize therapy remain difficult.1

Medical therapy for pulmonary arterial hypertension (PAH) is targeted directly toward the increased pulmonary artery (PA) pressures and high pulmonary vascular resistance. Typically, before starting treatment, a PAH patient’s baseline hemodynamics and acute vasoreactivity are evaluated with invasive monitoring during administration of a short-acting vasodilator such as IV epoprostenol, sodium nitroprusside, or inhaled nitric oxide. Fewer than 10% of IPAH patients have acute pulmonary vasoreactivity (ie, a decrease in mean PA pressure ≥ 10 mm Hg to ≤ 40 mm Hg with a normal or increased cardiac output during the acute test).1 The magnitude of the acute response, along with other clinical factors, is used to decide which therapy to initiate for an individual patient.2 The treatment goal, in addition to improving symptoms, is to reduce PA pressure and increase cardiac output without lowering systemic BP to a symptomatic level. Baseline invasive hemodynamic measurements have been shown to be useful in predicting outcome. The National Institutes of Health Primary Pulmonary Hypertension registry enrolled 194 patients and developed a prognostic equation for patients with IPAH.3 This equation took the form of A(x,y,z) = e(0.007325x) + (0.0526y) – (0.3275z), where x is mean PA pressure, y is mean right atrial pressure, and z is cardiac index obtained at the diagnostic cardiac catheterization. The probability of survival at 1, 2, and 3 years was P(1) = 0.75A, P(2) = 0.65A, and P(3) = 0.55A. However, this prognostic tool may underestimate survival in the current era following the advent of targeted IPAH therapy. This potential limitation can be overcome by serial invasive hemodynamic assessments to update hemodynamic data following initiation of therapy, although this exposes patients to repeated invasive procedures. An accurate and easily repeated method to follow serial hemodynamic parameters could be useful in assessing response to therapy and prognosis in IPAH. Recent investigations have used an implantable hemodynamic monitor (IHM) [Chronicle; Medtronic; Minneapolis, MN; a system limited to investigational use only] that records high-fidelity right ventricular (RV) pressure waveforms and provides estimates of mean PA pressure and right atrial pressure continuously.4 This device could be more useful if the tracking of the cardiac index was possible from RV pressure waveform because such development will allow estimation of all the parameters included in the prognostic equation.

It has been shown that not only the steady components (total pulmonary resistance) but also the oscillatory components of the RV afterload (characteristic impedance and pressure wave reflection) are also perturbed in IPAH patients.5 During acute vasodilator testing, as well as during chronic treatment, the therapy that increases cardiac output might reduce both these steady and oscillatory components of the RV afterload. These changes may or may not be accompanied by a significant decrease in mean PA pressure but may still influence the prognosis.

We have described a method to estimate cardiac output from the high-fidelity RV pressure waveform.6 Distinctly, this pulse contour cardiac output (PCCO) algorithm is not influenced by the presence of pressure wave reflection. This is important because the oscillatory components of the RV afterload (the amount of pressure wave reflection) could also be estimated through analysis of ventricular pressure waveforms.7 If accurate in IPAH patients, these techniques could broaden the range of hemodynamic data derived from RV pressure waveforms. In this study, we hypothesized that analysis of high-fidelity RV pressure waveforms might be useful in tracking the magnitude of pressure wave reflection and the cardiac index in patients with IPAH.

Materials and Methods

Patient Population and Inclusion/Exclusion Criteria
A Food and Drug Administration-regulated feasibility study of the potential utility of the Chronicle investigational device exemption in patients with IPAH (n = 24) is currently in process (IDE No. G020303). A subset of eight patients (mean age, 44 ± 5 years [± SD]; seven women and one man) who had a recent diagnosis of IPAH or were receiving stable IPAH therapy for at least 3 months were included in this study. The patients were ≥ 18 years of age, in World Health Organization functional class II-IV, and had an echocardiographically estimated PA systolic pressure > 50 mm Hg. They were enrolled in the study if, by appropriate evaluation, they had low probability of pulmonary embolism and were without parenchymal lung disease.2 Patients were also excluded if IPAH was related to left to right congenital systemic to pulmonary shunt, sickle-cell disease, HIV infection, schistosomiasis, left-sided valvular heart disease. or left ventricular dysfunction. In addition, patients were excluded from the study if their 6-min walk distance was < 50 m or > 450 m at baseline, or if they had another implantable device (pacemaker or defibrillator), or mechanical right-heart valve. The study was approved by Institutional Review Boards at participating facilities, and all patients provided written informed consent prior to enrollment.

Study Protocol
The IHM system was implanted in the left subclavicular region using standard sterile techniques used for pacemaker insertion. The RV lead was inserted via the subclavian vein and/or the internal jugular vein similar to insertion of standard transvenous pacemaker leads. The tip of the lead was in the RV outflow track, and the pressure sensor was 3 cm proximal to the tip.

At the time of the IHM implantation, the patients underwent acute vasodilator testing using IV epoprostenol at 3, 6, and 9 ng/kg/min for 10 min at each infusion dose. A Swan-Ganz oximetry catheter (Model 744HF75; Baxter Edwards Critical-Care; Irvine, CA) was placed with the tip in the PA to allow continuous measurements of mixed venous oxygen saturation by oximetry and also for the sampling of the blood. Arterial oxygen saturation was measured continuously by finger probe oximetry, and oxygen content was measured from an indwelling arterial line. Oxygen consumption was measured continuously, breath by breath, using a metabolic assessment system (CPX; Medgraphics; St Paul, MN). Because of the relatively long time constants associated with the Swan-Ganz system, we measured cardiac output provided by the metabolic assessment system. This system calculates breath-by-breath cardiac output according to the Fick principle, using mixed venous oxygen saturation from the optical Swan-Ganz catheter, arterial oxygen saturation from the finger probe oximeter, and oxygen consumption. The RV pressure waveforms and breath-by-breath cardiac index values, calculated as cardiac output divided by body surface area, were saved to a computer disk for subsequent analysis.

Feature Extraction and Data Analysis
Using proprietary software, 2 min of RV pressure waveform data were extracted at rest and with each epoprostenol dose. The RV pressure waveforms were analyzed to estimate the right atrial pressure (RV diastolic pressure [RVDP]), estimated PA mean pressure (eMPAP), estimated cardiac index (eCI), and the degree of wave reflection, denoted by the amplitude of the augmented pressure (AP) on a beat-by-beat basis. For this purpose, the following fiducial points on the RV pressure waveform were extracted using first and higher order pressure waveform derivatives using previously described methods789101112 (Fig 1 ), as follows: (1) the preejection interval (PEI), corresponding to maximum derivative of pressure measured over time (dP/dtmax)48101112; (2) the early shoulder pressure (Pfirst) of the RV pressure waveform, corresponding to the timing of peak flow and identified using higher order derivates of the RV pressure waveform79; (3) the peak RV pressure (Psys); and (4) the systolic time interval (STI) corresponding to minimum derivative of pressure measured over time (dP/dtmin).48 Accordingly, the RVDP was considered as the pressure at the onset of the R-wave, and the eMPAP was the weighted mean RV pressure between PEI and STI.4 The AP was calculated as the difference between the Psys and Pfirst.79


Figure 1
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  		Figure 1. Schematic representation of the basic features of the RV pressure waveform (top) and the identification of these feature points using the first derivative of the RV pressure waveform (middle). Three of these points identify the turning points of the PA flow waveform (bottom), PEI, Pfirst (P1st), and STI, where PEI = time of dP/dtmax, Pfirst = early systolic shoulder of the RV pressure waveform, and STI = time of dP/dtmin, respectively. The triangles inscribed in the RV pressure waveform and in the PA flow waveform denote the approximated and estimated flow contours, respectively. The RV AP caused by the presence of wave reflection is the difference between Psys and Pfirst. The ejection duration (ED) is defined as the difference between STI and PEI. EGM = electrogram.

 
Beat-by-beat eCI was calculated using a previously established RV pressure waveform-based PCCO algorithm.6 Briefly, this algorithm relies on the principle that the RV outflow contour can be identified in the RV pressure waveform. Considering that a triangle can be used to approximate the flow waveform, the eCI can be estimated as shown in Figure 1.

Formula 1(1)
where A is the body surface area, HR is the heart rate, and ED (ejection duration) and Formula 1max (peak volumetric flow) are the base and the apex of the triangle, respectively. The ED is calculated as the difference between PEI and STI489101112 (Fig 1, vertical dotted lines).

It has been previously shown that during early acceleration of blood flow, there is little presence of reflected waves579 and the rise of arterial pressure is simultaneous with the linear flow velocity. The characteristic impedance, Zc, which is a function of pulse wave velocity, blood density, and the cross-sectional area of the outflow tract, scales the magnitude of this pressure rise to that of volumetric flow velocity.613 It has been previously shown that Zc remains constant during a wide variety of conditions.5

Considering RV pressures at STI (Pes) and Pfirst, Formula 1max can be estimated from the RV pressure waveform as follows:

Formula 2(2)
The PCCO algorithm thus calculates eCI as follows:

Formula 3(3)
where the coefficient 1/Zc is considered to be a patient-specific "calibration factor" (see "Statistical Analysis" section) unaffected by changes in hemodynamics. Note that if the value of Zc is unknown, equation 3 denotes the cardiac index normalized to Zc.

Statistical Analysis
Because cardiac index measured by the breath-by-breath technique (mCI) was highly variable (mean ± SD, 46 ± 15%), the measured and estimated parameters were averaged and analyzed in bins (2 min, 233 ± 17 beats/bin) corresponding to rest and epoprostenol dose. The so-called patient-specific "calibration factor" (the coefficient 1/Zc in equation 3) was estimated using a multiple linear regression model.14 This model takes into account the presence of individual patient differences and the epoprostenol doses in the final equation (ie, this model assumes that each patient may have an individual calibration factor as determined by their physiologic and anatomic properties). The resultant multiple correlation coefficient of this model was considered to be the measure of linearity and an estimate of the quality of the PCCO algorithm. A theoretical background, applications, and limitations of multiple linear regression analysis can be found in Slinker and Glantz.14

The baseline hemodynamic parameters and the dose effects were also assessed using the multiple linear regression model described above. The Bland-Altman analysis was performed to assess the bias and agreement of the eCI compared to mCI.15

Analyses were performed using a commercially available statistical package (Axum 4.0; Mathsoft; Cambridge, MA). Data are expressed as the mean ± SEM unless otherwise noted; p values < 0.05 were considered statistically significant.

Results

The beat-to-beat RV waveform features in one patient during IV epoprostenol infusion are displayed in a color-encoded format in Figure 2 , left, A, where waveforms from each successive beats are stacked. At baseline, RV pressure contours exhibited early shoulders at 52 ± 0.2 mm Hg (Pfirst; Fig 2, bottom right, B). During late systole, the RV pressure increased further to a second shoulder, marking the systolic pressure of 79 ± 0.2 mm Hg (Psys; color coded in red in Fig 2). Hence, the RV pressure augmentation averaged 28 ± 0.2 mm Hg at baseline. At the IV epoprostenol dose of 3 ng/kg/min, the early systolic shoulder pressure decreased to 39 ± 0.2 mm Hg, although this was less than the reduction in RV systolic pressure to 55 ± 0.2 mm Hg (Fig 2, center right, C). The reduction in augmented pressure contributed to the reduction in systolic pressure. At the highest dose attained in this patient (6 ng/kg/min), the late systolic RV pressure augmentation (16 ± 0.2 mm Hg) and the RV systolic pressure remained low (53 ± 0.2 mm Hg). After ending the IV epoprostenol infusion, both the late RV systolic pressure augmentation and the RV systolic pressure increased, although not to the baseline levels during the time of this recording (Fig 2, top right, D).


Figure 2
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  		Figure 2. Left, A: Beat-to-beat RV pressures encoded in color to aid the visualization of the effect of epoprostenol in one patient (patient 2). Shown are representative waveforms at selected time points (arrows): top right, D; center right, C; and bottom right, B. The points of the RV pressure waveform that are used by the PCCO algorithm are highlighted (bottom right, B) and shown as a continuous line (left, A). Late RV systolic pressure augmentation in high during baseline and reduced during drug infusion.

 
Although respiratory rate (19 ± 1 breaths/min), arterial oxygen saturation (92 ± 1%), and oxygen consumption (3.1 ± 0.2 mL/min/kg) did not change from baseline with epoprostenol infusion, heart rate (90 ± 1 beats/min), mixed venous oxygen saturation (58 ± 1%), and cardiac index increased significantly with the highest dose of epoprostenol (10 ± 2 beats/min, 11 ± 2%, and 1.2 ± 0.3 L/min/m2, respectively; p < 0.01 for all). This increase in cardiac index at the highest dose was accompanied by an absence of change in RV filling pressure, in mean PA pressure (Table 1 ), and in RV contractility (as assessed by RV dp/dtmax, data not shown). These findings suggested RV afterload is reduced with epoprostenol infusion. Indeed, the total pulmonary vascular resistance index (from 38 ± 2 to 23 ± 4 Wood U/m2, p < 0.001) and the augmented pressure in the RV (from 29 ± 1 to 22 ± 2 mm Hg, p < 0.05) were both decreased (Table 1).


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  		Table 1. RV Pressure Waveform-Derived Parameters*

 
The Fick cardiac index in one patient (patient 4) during varying doses of IV epoprostenol infusion is shown in Figure 3 . Notice that in this presentation, mCI and eCI data were averaged and analyzed in bins of 1 min. The Fick cardiac index at baseline was 1.7 ± 0.7 L/min/m2 and increased to 4.6 ± 3.0 L/min/m2 with 9 ng/kg/min of IV epoprostenol.


Figure 3
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  		Figure 3. mCI and PCCO eCI in one patient (patient 4) during the course of one study. Arrows indicate the samples obtained at baseline, and at 3, 6, and 9 ng/kg/min epoprostenol infusion rates. The data are averaged over 1 min to reduce the effects of respiration.

 
The multiple linear regression model indicated that eCI estimated using the PCCO method had different calibration factors for each patient. Despite the existence of these patient dependent calibration factors, the measured and the estimated values of total pulmonary vascular resistance index changed in the same direction with epoprostenol infusion (Table 1). Once these patient-dependent calibration factors were taken into account, the eCI by the PCCO method continuously tracked the changes in mCI: mCI (L/min/m2) = 1 x eCI (L/min/m2); r2 = 0.95, p < 0.001; Fig 4 , left, A. The Bland-Altman analysis indicated the absence of proportional bias of the estimate (0.0 L/min/m2; Fig 4, bottom right, B). The SD of the differences was 0.18 L/min/m2.


Figure 4
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  		Figure 4. Top: Linear regression line for mCI and eCI together with the 95% confidence bounds (CI) of the equation. Bottom: Bland-Altman plot depicting the agreement between mCI and eCI.

 
Discussion

In this study, we analyzed high-fidelity RV pressure waveforms recoded with an IHM to continuously track hemodynamic parameters (ie, mean PA pressure, right atrial pressure, and cardiac index) that are thought to be prognostic predictors in patients with IPAH during acute epoprostenol infusion. We also analyzed RV pressure waveforms to estimate the magnitude of pressure wave reflection in these patients. We found that RV pressure waveform analysis provides reliable estimates of these hemodynamic parameters. Specifically, we found that the PCCO algorithm, which takes into account the influence of wave reflection, tracked the Fick cardiac index accurately.

A major impediment to optimizing drug regimens in PAH patients is the need to perform serial invasive procedures to assess pulmonary and systemic hemodynamics. The IHM device currently being evaluated can provide clinicians with the ability to monitor RV pressures on a continuous basis.4161718 In addition to these benefits, the PCCO algorithm described in this study may be useful to track cardiac index and total pulmonary vascular resistance index during changes in treatment regimens. Potentially, the changes in RV waveform morphology reflected in measures such as late RV systolic pressure augmentation may give further insights into how the pulmonary vascular changes relate to the changes in pulmonary impedance.57192021

At baseline, as expected, the IPAH patients in this study had high RV systolic and eMPAP consistent with the values from the Swan-Ganz catheter (data not shown). We found that in these patients, both the steady (total pulmonary vascular resistance) and oscillatory components (as assessed by the late RV systolic pressure augmentation) are important contributors to RV afterload. This finding is consistent with an earlier report5 in a similar group of patients undergoing a structured exercise test.

It is usually assumed that decreased RV systolic pressure or decreased pulsatility of the RV pressure waveform suggests a reduced stroke volume. However, in this study, the RV systolic pressure decreased in the absence of a change in mean pulmonary artery pressure with a concomitant increase in cardiac index. This decrease in systolic pressure was minor (approximately 15%) compared to the reduction in total pulmonary vascular resistance (approximately 40%). Interestingly, decreased wave reflection (as assessed by the AP) and increase in stroke volume might explain this finding. The data from this study suggest that reliance on traditional measures of RV or PA pressures may not provide a complete hemodynamic picture. Analysis of RV pressure waveforms to obtain an estimate of cardiac index and magnitude of wave reflection might mitigate some of these concerns.

Limitations
At the highest dose of IV epoprostenol infusion, we observed a similar reduction in the left ventricular afterload to RV afterload, as assessed by the total systemic and pulmonary resistance indexes. Although we cannot rule out that the observed improvement in cardiac index might also be due to reduced left ventricular afterload, the predominant benefit was due to an improvement in ventricular/vascular coupling on the right side (unpublished data).19

Because precise determinations of feature points are needed to conduct the analyses described in this study, use of a high-fidelity pressure recording system is important. Although we employed an IHM device in this study, alternative high-fidelity micromanometer systems but not fluid-filled catheters could also be used for this purpose. However, IHM has the potential to provide continuous estimates of relevant hemodynamic parameters in chronic settings.

We measured total pulmonary vascular resistance index, as opposed to pulmonary vascular resistance index, which considers the magnitude of the pulmonary capillary wedge pressure. In this group of patients, the IHM does not provide direct measure of pulmonary capillary wedge pressure. However, baseline pulmonary capillary wedge pressures in these patients were low (< 15 mm Hg).

The PCCO algorithm used in this study requires extraction of features from the RV pressure waveform corresponding to the features of the PA flow waveform. We relied on the first derivative of RV pressure waveform to estimate the onset, peak, and cessation of the RV outflow. It has been shown that these features can be identified from the RV pressure waveform.48101112 Although patients with tricuspid valve disease were included in the study by Chuang et al,10 the presence of significant pathologic pulmonary and tricuspid valve diseases and arrhythmias might affect these results.

The PCCO algorithm considers that the characteristic impedance of the RV outflow track remains constant for a given individual.6 Although it has been reported that this parameter of the PA is almost constant in various settings,52021 this could contribute to the variability of the eCIs.

Conclusions

In patients with IPAH, the analysis of RV pressure waveform provides information that could be useful to assess clinical status, response to therapy, and prognosis. From the RV pressure waveform, right atrial pressure, mean pulmonary artery pressure, and systolic pulmonary artery pressures can be estimated. In addition, further analysis of RV pressure yields additional clinical indexes such as the change in magnitude of wave reflection and cardiac index during acute therapeutic interventions. The potential to accurately and repeatedly measure cardiac index utilizing an implantable monitor could have important implications for serial assessment of therapeutic regimens and prognosis in patients with IPAH.

Acknowledgements

We gratefully acknowledge the clinical and technical assistance of Cathy J. Severson, RN, and Lisa Fanning.

Footnotes

Abbreviations: AP = augmented pressure; dP/dtmax = maximum derivative of pressure measured over time; dP/dtmin = minimum derivative of pressure measured over time; eCI = estimated cardiac index; eMPAP = estimated pulmonary artery mean pressure; IHM = implantable hemodynamic monitor; IPAH = idiopathic pulmonary arterial hypertension; mCI = cardiac index measured by the breath-by-breath technique; PA = pulmonary artery; PAH = pulmonary arterial hypertension; PCCO = pulse contour cardiac output; PEI = preejection interval; Pes = right ventricular pressure at systolic time interval; Pfirst = early shoulder pressure; Psys = peak RV pressure; Formula 3max = peak volumetric flow; RV = right ventricular; RVDP = right ventricular diastolic pressure; STI = systolic time interval

This study was supported by Medtronic, Inc. The authors have acted as consultants to Medtronic, Inc. (M.M., R.C.B.), and have received research funding from Medtronic, Inc. (M.M., R.P.F., R.J.B., and R.L.B.).

Received for publication November 6, 2006. Accepted for publication March 15, 2007.

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