Estimation of cardiac output in patients with congestive heart failure by analysis of right ventricular pressure waveforms.

BACKGROUND: Cardiac output (CO) is an important determinant of the hemodynamic state in patients with congestive heart failure (CHF). We tested the hypothesis that CO can be estimated from the right ventricular (RV) pressure waveform in CHF patients using a pulse contour cardiac output algorithm that considers constant but patient specific RV outflow tract characteristic impedance. METHOD: In 12 patients with CHF, breath-by-breath Fick CO and RV pressure waveforms were recorded utilizing an implantable hemodynamic monitor during a bicycle exercise protocol. These data were analyzed retrospectively to assess changes in characteristic impedance of the RV outflow tract during exercise. Four patients that were implanted with an implantable cardiac defibrillator (ICD) implementing the algorithm were studied prospectively. During a two staged sub-maximal bicycle exercise test conducted at 4 and 16 weeks of implant, COs measured by direct Fick technique and estimated by the ICD were recorded and compared. RESULTS: At rest the total pulmonary arterial resistance and the characteristic impedance were 675 ± 345 and 48 ± 18 dyn.s.cm(-5), respectively. During sub-maximal exercise, the total pulmonary arterial resistance decreased (Δ 91 ± 159 dyn.s.cm(-5), p < 0.05) but the characteristic impedance was unaffected (Δ 3 ± 9 dyn.s.cm(-5), NS). The algorithm derived cardiac output estimates correlated with Fick CO (7.6 ± 2.5 L/min, R(2) = 0.92) with a limit of agreement of 1.7 L/min and tracked changes in Fick CO (R(2) = 0.73). CONCLUSIONS: The analysis of right ventricular pressure waveforms continuously recorded by an implantable hemodynamic monitor provides an estimate of CO and may prove useful in guiding treatment in patients with CHF.

Estimating changes in cardiac output using an implanted hemodynamic monitor in heart failure patients.

OBJECTIVES: The aim of this study was to evaluate an algorithm that estimates changes in cardiac output (CO) from right ventricular (RV) pressure waveforms derived from an implantable hemodynamic monitor (IHM) in heart failure patients. DESIGN: Twelve heart failure patients (NYHA II-III, EF 32%) with an implantable hemodynamic monitor (Chronicle) were included in this study. Changes in cardiac output were provoked by body position change at rest (left lateral supine, horizontal supine, sitting, and standing) and a steady state bicycle exercise at 20 watts. Estimated CO derived from the IHM (CO(IHM)) was compared to CO measured with inert gas rebreathing (CO(RB)), echocardiography (CO(ECHO)) and impedance cardiography (CO(ICG)). CO(RB) was considered the reference method. RESULTS: The median intra-patient correlation coefficient comparing CO(RB) and CO(IHM) was 0.83 (range: 0.63-0.98). Comparing CO(RB) with CO(ECHO) and CO(ICG) resulted in mean intra-patient correlation coefficients of 0.73 (-0.29-0.94) and 0.63 (-0.29-0.96). In a statistical model where slope and intercept was considered random between patients the coefficient of determination (R2) comparing CO(RB) and CO(IHM) was 0.91. Mean bias was -0.39 L/min (11%). Limits of agreement were +/-1.56 L/min and relative error was 21%. CONCLUSIONS: A simple algorithm based on RV pressure wave form characteristics derived from an IHM can be used to estimate changes in CO in heart failure patients. These findings encourage further research aiming to improve and validate the algorithm.

Characterization of the upper limb arterial properties during reactive hyperemia.

The radial artery (RA) pressure waveform is commonly used to reconstruct the central aortic pressure waveform. Because the RA pressure waveform has been used as input to this process, its features that are dependent on the local arterial properties can influence the final reconstructed aortic waveform. In this study, we determined the effects of altered upper limb pulse wave velocity (PWV) and local wave reflection parameters on RA pressure waveform augmentation (RA-AIx). Twenty healthy volunteers (10 men) between the ages of 18 and 35 years of age were recruited. Simultaneous pressure waveforms were acquired using arterial tonometers from the right carotid and the radial arteries, prior to and following tourniquet induced hyperemia. The phase velocities from the pressure wave transfer function were used to estimate the pulse wave velocity (PWV(infinity)), the local reflection coefficient (Gamma) and an estimate of the terminal impedance of the upper limbs, PWV(0+). The RA-AIx was represented as a linear, three-parameter model that included the input (the AIx of the carotid artery pressure waveform, CA-AIx), the Gamma and PWV(infinity) of the arm. Tourniquet induced hyperemia did not alter Gamma but reduced PWV(infinity), and PWV(0+) and increased RA-AIx. Multiple linear regression analysis indicated that RA-AIx was increased by high levels of CA-AIx and PWV(infinity) and decreased by elevated Gamma. The relative weighing of CA-AIx, Gamma and PWV(infinity) on RA-AIx were 3:2:1, respectively. The AIx of RA is determined to an equal extent by the input and local factors. Interpretation of the AIx of the RA and the reconstructed central aortic waveform should be made in the context of this relationship.

Right ventricular pressure waveform and wave reflection analysis in patients with pulmonary arterial hypertension.

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/m(2), total pulmonary resistance index was 38 +/- 2 Wood U/m(2), 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/m(2), 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 (r(2) = 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.

A right ventricular pressure waveform based pulse contour cardiac output algorithm in canines.

Tracking changes in stroke volume or cardiac output (CO) can be useful in the diagnosis and treatment of various cardiac illnesses. Existing arterial pressure waveform based pulse contour CO algorithms perform poorly during altered systemic hemodynamics. In this study, a right ventricular pressure waveform based pulse contour CO algorithm was developed to estimate the amplitude and duration of a hypothetical triangular flow waveform in the pulmonary artery. This algorithm was tested against gold standard blood flow measurements in ten canines during acute perturbations to preload (inferior vena caval occlusion (IVCO), rapid saline infusion), afterload (descending aortic occlusion (DAO), serotonin, angiotensin II, sodium nitroprusside infusion), and cardiac contractility (dobutamine and propranolol infusion). The algorithm correctly predicted the changes in CO (r2 = 0.82) that varied from - 45 to 31% of the baseline levels. To explain this finding both the pulmonary arterial (PA) and the ascending aortic (AA) input impedances were modeled as three element windkessels. In the AA the peripheral resistance (from - 61 to 191%), characteristic impedance (from - 59 to 20%) and total arterial compliance (from - 49 to 34%) varied significantly with these perturbations. In contrast, these parameters in the PA changed little. In particular, except serotonin infusion, the characteristic impedance of the PA deviated only 6% (SD/mean) from baseline values. This suggests right ventricular pressure waveform based estimate of CO is possible during acute changes in left ventricular hemodynamics.

The peak atrioventricular pressure gradient to transmitral flow relation: kinematic model prediction with in vivo validation.

Physiologists and cardiologists estimate peak transvalvular pressure gradients (DeltaP) by Doppler echocardiographic imaging of peak flow velocities using the simplified Bernoulli relationship: DeltaP (mm Hg) = 4V(2) (m/s). Because left ventricular filling is initiated by mechanical suction, V can be predicted by the motion of a simple harmonic oscillator by the parametrized diastolic filling formalism that characterizes E-wave contours by 3 unique simple harmonic oscillator parameters: initial displacement (x(o) cm); spring constant (k g/s(2)); and damping constant (c g/s). Parametrized diastolic filling predicts peak atrioventricular pressure gradient as kx(o), the peak simple harmonic oscillator force. For validation, simultaneous (micromanometric) left ventricular pressure and E-wave data from 19 patients were analyzed. Model-predicted peak gradient (kx(o)) was compared with actual gradient (DeltaP(cath)) and with 4V(2). Multiple linear regression results for all patients yielded highly significant relation between kx(o) and DeltaP(cath) (kx(o) = m(1)DeltaP(cath) + b(1), where m(1) = 40.7 +/- 8.0 dyne/mm Hg, b(1) = 1540 +/- 116 dyne, r(2) = 0.97, P <.001). Regression analysis showed no significant correlation between 4V(2) and DeltaP(cath) (4V(2) = m(2)DeltaP(cath) + b(2), where m(2) = 0.01 +/- 0.03, m(2)/s(2)/mm Hg and b(2) = 2.07 +/- 0.44 m(2)/s(2), P = nonsignificant). We conclude that E-wave analysis by parametrized diastolic filling predicts peak atrioventricular gradients reliably and more accurately than 4V(2).

Left ventricular chamber stiffness at rest as a determinant of exercise capacity in heart failure subjects with decreased ejection fraction.

Impaired exercise tolerance, determined by peak oxygen consumption (VO2 peak), is predictive of mortality and the necessity for cardiac transplantation in patients with chronic heart failure (HF). However, the role of left ventricular (LV) diastolic function at rest, reflected by chamber stiffness assessed echocardiographically, as a determinant of exercise tolerance is unknown. Increased LV chamber stiffness and limitation of VO2 peak are known correlates of HF. Yet, the relationship between chamber stiffness and VO2 peak in subjects with HF has not been fully determined. Forty-one patients with HF New York Heart Association [(NYHA) class 2.4 +/- 0.8, mean +/- SD] had echocardiographic studies and VO2 peak measurements. Transmitral Doppler E waves were analyzed using a previously validated method to determine k, the LV chamber stiffness parameter. Multiple linear regression analysis of VO(2 peak) variance indicated that LV chamber stiffness k (r2 = 0.55) and NYHA classification (r2 = 0.43) were its best independent predictors and when taken together account for 59% of the variability in VO2 peak. We conclude that diastolic function at rest, as manifested by chamber stiffness, is a major determinant of maximal exercise capacity in HF.

Duration of diastole and its phases as a function of heart rate during supine bicycle exercise.

The duration of diastole can be defined in terms of mechanical events. Mechanical diastolic duration (MDD) is comprised by the phases of early rapid filling (E wave), diastasis, and late atrial filling (A wave). The effect of heart rate (HR) on diastolic duration is predictable from kinematic modeling and known cellular physiology. To determine the dependence of MDD of each phase and the velocity time integral (VTI) on HR, simultaneous transmitral Doppler flow velocities and ECG were recorded during supine bicycle exercise in healthy volunteers. Durations, peak values, and VTI using triangular approximation for E- and A-wave shape were measured. MDD, defined as the interval from the start of the E wave to end of the A wave, was fit as an algebraic function of HR by MDD=BMDD + MLMDD.HR + MIMDD/HR, derivable from first principles, where BMDD is a constant, and MLMDD and MIMDD are the constant coefficients of the linear and inverse HR dependent terms. Excellent correlation was observed (r2=0.98). E- and A-wave durations were found to be very nearly independent of HR: 100% increase in HR generated only an 18% decrease in E-wave duration and 16% decrease in A-wave duration. VTI was similarly very nearly independent of HR. Diastasis duration closely tracked MDD as a function of HR. We conclude that the elimination of diastasis and merging of E and A waves of nearly fixed durations primarily govern changes in MDD. These observations support the perspective that E- and A-wave durations are primarily governed by the rules of mechanical oscillation that are minimally HR dependent.

Thermodynamic phase plane analysis of ventricular contraction and relaxation.

BACKGROUND: Ventricular function has conventionally been characterized using indexes of systolic (contractile) or diastolic (relaxation/stiffness) function. Systolic indexes include maximum elastance or equivalently the end-systolic pressure volume relation and left ventricular ejection fraction. Diastolic indexes include the time constant of isovolumic relaxation - and the end-diastolic pressure-volume relation. Conceptualization of ventricular contraction/relaxation coupling presents a challenge when mechanical events of the cardiac cycle are depicted in conventional pressure, P, or volume, V, terms. Additional conceptual difficulty arises when ventricular/vascular coupling is considered using P, V variables. METHODS: We introduce the concept of thermodynamic phase-plane, TPP, defined by the PdV and VdP axes. RESULTS: TPP allows all cardiac mechanical events and their coupling to the vasculature to be geometrically depicted and simultaneously analyzed. CONCLUSION: Conventional systolic and diastolic function indexes are easily recovered and novel indexes of contraction-relaxation coupling are discernible.