Peripheral Pressure Waveform Research Articles

The Accuracy of Central Systolic Blood Pressure Determined from the Second Systolic Peak of the Peripheral Pressure Waveform

The Accuracy of Central Systolic Blood Pressure Determined from the Second Systolic Peak of the Peripheral Pressure Waveform

The accuracy of central SBP determined from the second systolic peak of the peripheral pressure waveform

Recent evidence suggests that central aortic blood pressure may be a better predictor of cardiovascular risk than peripheral blood pressure. The central SBP (cSBP) can be estimated from the late systolic shoulder of the radial pulse waveform. We compared the second systolic peak of the radial waveform (pSBP(2)) with the central systolic pressure derived by a generalized transfer function in a large cohort, across a wide age range, of patients from the Anglo-Cardiff Collaborative Trial. We also compared pSBP(2) with the true cSBP measured by cardiac catheterization [invasively measured cSBP (cSBPi)]. Noninvasive measurements were made by applanation tonometry using the SphygmoCor device. The aortic pressure waveform was derived from the radial waveform using a validated transfer function. Invasive measures of cSBPi were carried out in a group of 38 patients undergoing diagnostic cardiac angiography, and radial artery pressure waveforms were simultaneously recorded using the SphygmoCor device. Overall, there was a strong correlation (r = 0.99, P<0.001) and good agreement between pSBP(2) and the derived cSBP (mean difference +/- SD 1 +/- 4 mmHg). However, there was a systematic bias with a greater difference between these measures at lower average pressures. There was also a strong correlation and good agreement between the invasively measured cSBPi and pSBP(2) (r = 0.92, P<0.001, mean difference 2 +/- 6 mmHg). The second systolic shoulder of the peripheral pressure waveform approximates the cSBP in a large cohort of patients across a wide age range, but this may be inaccurate at low SBP values.

Pressure Waves as a Noninvasive Tool for Artery Stiffness Estimation

In hypertension and aging, central elastic arteries become stiffer and hence the central pulse pressure is augmented due to the increase in the pulse wave velocity and the early return of reflected waves to the heart from the periphery. Valuable information on arterial properties, such as stiffness, can be obtained from both central (aortic) and peripheral (radial) pressure wave forms. A feasibility study for the noninvasive estimation of arterial stiffness using pressure waves detected by a pneumatic cuff wrapped around the upper arm is presented. The propagation and reflection of arterial pressure waves (generated by the heart) in the central elastic arteries are simulated using a simplified water hammer acoustic model. Furthermore, a lumped parameter model is used to describe the transmission of the pressure waves from the brachial artery to the cuff external wall. By combining the two models, we were able to simulate the pressure contours in the brachial artery and illustrate how these pressures transmit to the cuff’s external wall. The effects of aortic stiffness are investigated by simulating the model at different values of aortic elastic moduli and observing the pressure augmentation and the timing of feature points. This work was done as part of the development of a noninvasive diagnostic device by Pulsecor Ltd. The model results obtained in this work are in agreement with published experimental results and the device output; hence, the model can be used to develop the device’s stiffness estimation algorithm.

Peripheral Augmentation Index Defines the Relationship Between Central and Peripheral Pulse Pressure

Peripheral systolic blood pressure is amplified above central aortic systolic pressure, but the late systolic shoulder of the peripheral pulse may approximate central systolic pressure. Because late systolic pressure also determines the peripheral augmentation index, a measure of pressure wave reflection within the systemic circulation, this implies a direct relationship between amplification and augmentation. We compared the late systolic shoulder of the peripheral pressure waveform with estimates of central systolic pressure obtained using a transfer function in 391 subjects undergoing diagnostic coronary angiography and/or elective angioplasty (30% with insignificant coronary artery disease). In a subset (n=12) we compared the late systolic shoulder of the peripheral pulse with central pressure obtained with a catheter placed in the aortic root. Measurements were made at baseline, during atrial pacing, and during administration of nitroglycerin. Late systolic shoulder pressure closely approximated transfer function estimates of central pressure (R=0.96; P<0.0001; mean difference+/-SD: 0.5+/-5.2 mm Hg). Despite changes in waveform morphology induced by pacing and nitroglycerin (reducing mean values+/-SE of the augmentation index from 76+/-3.8% to 66+/-4.6% and 60+/-3.3%, respectively), there was close agreement between the late systolic shoulder of the peripheral pulse and measured values of central pressure (R=0.96; P<0.001; mean difference: 1.7+/-4.8 mm Hg). In conclusion, the late systolic shoulder of the peripheral pulse closely approximates central systolic pressure and peripheral augmentation index, the ratio of central:peripheral pulse pressure. Interventions to lower augmentation index and peripheral vascular resistance will have multiplicative effects in lowering central blood pressure.

Laguerre-Model Blind System Identification: Cardiovascular Dynamics Estimated From Multiple Peripheral Circulatory Signals

This paper presents a method for comparing multiple circulatory waveforms measured at different locations to improve cardiovascular parameter estimation from these signals. The method identifies the distinct vascular dynamics that shape each waveform signal, and estimates the common cardiac flow input shared by them. This signal-processing algorithm uses the Laguerre function series expansion for modeling the hemodynamics of each arterial branch, and identifies unknown parameters in these models from peripheral waveforms using multichannel blind system identification. An effective technique for determining the Laguerre base pole is developed, so that the Laguerre expansion captures and quickly converges to the intrinsic arterial dynamics observed in the two circulatory signals. Furthermore, a novel deconvolution method is developed in order to stably invert the identified dynamic models for estimating the cardiac output (CO) waveform from peripheral pressure waveforms. The method is applied to experimental swine data. A mean error of less than 5% with the measured peripheral pressure waveforms has been achieved using the models and excellent agreement between the estimated CO waveforms and the gold standard measurements have been obtained.

Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms

Aortic pulse wave velocity (PWV) and augmentation index are independent predictors of adverse cardiovascular events, including mortality. In hypertension and aging, central elastic arteries become stiffer, diastolic pressure decreases, and central systolic and pulse pressures are augmented due to increased PWV and early return of reflected waves to the heart from the periphery. Valuable information on arterial properties such as stiffness can be obtained from both central (aortic) and peripheral (radial artery) pressure waveforms, but absolute values of wave reflection amplitude and wasted left ventricular (LV) pressure energy can only be obtained from the central arterial pressure waveform. As the arterial system becomes stiffer, there is a marked increase in central systolic and pulse pressures and wasted LV energy, along with a decrease in pulse pressure amplification. The increase in aortic systolic and pulse pressures are due primarily to increases in PWV and wave reflection amplitude with a small increase in incident wave amplitude. In individuals with very stiff elastic arteries (eg, in older persons with isolated systolic hypertension), there is a decrease in diastolic pressure. These changes in pressure components increase LV afterload and myocardial oxygen demand and therefore cause an undesirable mismatch between ventricle emptying and arterial pulse wave transmission, which promotes ventricular hypertrophy. High systolic and pulse pressures resulting from advanced age or hypertension increase circumferential arterial wall stress, which likely causes breakdown of medial elastin and increases the possibility of local fatigue, endothelial damage and development of atherosclerosis. Vasodilator drugs may have little direct effect on large central elastic arteries, but at the same time, their effects on peripheral muscular arteries reduce wave reflection amplitude and markedly lower systolic and pulse pressures and ventricular afterload. These beneficial effects on central arterial pressure can occur with or without a reduction in cuff blood pressure (BP) and may explain the apparent "pressure-independent" effects of drugs such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Therefore, optimal treatment of high BP and its complications should include consideration of arterial stiffness, augmentation of aortic pressure, and LV wasted energy, all of which should be reduced to the lowest possible level.

Adaptive left ventricular ejection time estimation using multiple peripheral pressure waveforms.

An adaptive approach is proposed for the problem of left ventricular ejection time (LVET) estimation using peripheral pressure waveform signals. The proposed algorithm, which makes use of 2 peripheral pressure measurements, makes it possible to adaptively estimate the LVET in response to different cardiovascular physiologic states. The algorithm builds on features obtained from global and branch-specific characterization of the cardiovascular circulation as well as waveform features to dramatically improve the accuracy of LVET estimation. The performance of the proposed approach is evaluated with respect to its heart-rate-based conventional counterpart, which shows approximately 40% improvement of estimation accuracy in terms of R2values □ from 0.6655 for the conventional waveform-based approach to 0.9222 for the proposed approach.

Assessment of endothelial function using peripheral waveform analysis: A clinical application

ObjectivesThe study was done to determine whether radial artery applanation tonometry can be used as a noninvasive method of assessing global endothelial function. BackgroundIt is known that beta2-receptor stimulation results in endothelial release of nitric oxide. Furthermore, for over a century glyceryl trinitrate (GTN) has been known to markedly affect the arterial pressure waveform, even in the absence of significant blood pressure (BP) changes. Therefore, it was hypothesized that the change in the peripheral pressure waveform, as measured using tonometry and quantified using the augmentation index (AIx) and in response to Salbutamol (Salb), would allow assessment of global endothelial function. MethodsThe study contained three parts. In the first study, Salb (400 μg) was administered to 11 healthy subjects via inhalation after either intravenous N-ω-nitro-monomethyl-l-arginine (l-NMMA) (3 mg/kg over 5 min) or control solution (normal saline) in the supine, rested, fasted condition. The BP, heart rate and waveform responses were recorded each 5 min following Salb for 20 min. Next, GTN was given and responses recorded 5 min later. In the second study, both the reproducibility of Salb and the GTN responses were assessed in 9 subjects studied twice on separate days. In the third study, the Salb and GTN responses of 12 subjects with angiographic coronary artery disease (CAD) were compared with 10 age-matched control subjects with no atherosclerotic risk factors. ResultsAfter control infusion, AIx decreased following Salb, from 50.8 ± 4.3% to 44.8 ± 4.2%, a change of −11.8 ± 3.7%, p < 0.01. After l-NMMA, AIx did not significantly change following Salb (54.2 ± 5.1% vs. 52.9 ± 5.3%, −2.0 ± 3.1%). The GTN-induced decreases in AIx were similar after either infusion (35.1 ± 3.3% vs. 36.5 ± 3.3%). Reproducibility of Salb-induced changes in AIx between studies performed on separate days was good (r = 0.80, p < 0.01). Salb-induced changes in AIx in CAD patients were significantly less compared to control subjects (−2.4 ± 1.9% vs. −13.2 ± 2.4%, respectively, p < 0.002). The GTN-induced changes were not significantly different (−27.6 ± 4.2 vs. −38.9 ± 4.4%, p = 0.07). ConclusionsThe peripheral arterial pressure waveform is sensitive to beta2-stimulation. Changes are related to nitric oxide release, are reproducible and can distinguish between clinical subject groups. Arterial waveform changes following Salb may thus provide a noninvasive method of measuring “global” arterial endothelial function.

The effects of thyrotoxicosis and its treatment on central arterial stiffness.

To assess central arterial stiffness in thyrotoxicosis using the technique of pulse wave analysis. Case control study designed to determine the effect of thyrotoxicosis on central arterial stiffness and at 6 months after radioiodine treatment. Twenty (18 women and 2 men) thyrotoxic patients and 20 age- and sex-matched controls were studied at baseline. Thyrotoxic patients were re-studied at 6 months following treatment of thyrotoxicosis with 555 MBq (131)I with no additional therapy for the six-month period. Using the sphygmocor apparatus, peripheral pressure waveforms were recorded non-invasively from the radial artery and central pressure waveforms were generated from these. Indices of arterial stiffness, central augmentation index (AI), augmentation of central arterial pressure (AG) and central blood pressures were derived. AI corrected for heart rate (AIc) was calculated. Thyrotoxic patients recorded a significantly lower AI (means+/-s.e.m.) compared with controls (15.0+/-2.1 vs 28.0+/-2.1%; P<0.0005) even when corrected for differences in heart rate AIc (20.0+/-2.1 vs 28.0+/-2.1%; P<0.005) as well as AG (6.0+/-0.8 vs 10.0+/-1.1 mmHg; P<0.002) but higher pulse pressure (58.0+/-3.5 vs 47.0+/-2.0 mmHg; P<0.02). At 6 months following treatment, a significant rise in AIc (27.0+/-1.8 vs 20.0+/-2.1%; P<0.005) and AG (11.0+/-1.0 vs 6.0+/-0.8 mmHg; P<0.005) was noted. Lipid profiles were comparable between the groups. These data suggested that subjects with untreated thyrotoxicosis have a decreased augmentation of central arterial pressure or lowered central arterial stiffness that would not appear to contribute to any excess cardiovascular risk in that condition.

Estimation of Arterial Mechanical Properties from Aortic and Tonometric Arterial Pressure Waveforms

Although arterial mechanical properties have been evaluated using arterial input impedance, the relative difficulty in accurate flow measurement made the value of impedance somewhat limited. To develop an alternative method to evaluate arterial mechanical properties, we analyzed the aortic pressure (AoP)-radial arterial pressure (RAP) relationship because of relative ease in obtaining peripheral pressure waveform by tonometry. In 8 patients we simultaneously recorded aortic root and radial arterial pressure waveforms. We calculated the transfer function from AoP to RAP. We then fitted the transfer function to a model of a lossless uniform elastic tube terminated with a modified Windkessel model. The fact that the model transfer function predicted AoP from RAP waveform with considerable accuracy indicated that the model represented the arterial mechanical properties well. We conclude that we can estimate the arterial mechanical properties by the pressure-pressure transfer function analysis.

A model of the carotid vascular system with stenosis at the carotid bifurcation

Stroke is one of the major diseases leading to human death and may be caused by arterial stenosis, possibly combined with arterial spasm. Carotid stenosis can be detected through ocular pulse caused by the blood flow in the choroid which, in turn, is influenced by the blood flow in the carotid vascular system (CVS). This paper presents a mathematical model of the stenosis, usually located at the carotid bifurcation into the external and internal carotid arteries. The model is based on experimental data from in vitro studies. The stenosis is modelled as a nonlinear resistive element, causing a pressure drop in the blood flow over a local constriction. Such a pressure change affects the spectral contents of peripheral pressure waveforms, particularly the ocular blood pressure (OBP) waveform. The dynamics of the CVS with stenosis is determined by the haemodynamic and geometric properties of the stenosis. Computer implementation and simulation of the composite model shows how the OBP waveform dynamics is affected by the level of the stenosis. These unique results are being used in our research on a method for early detection of stroke, glaucoma, and elevated intracranial pressure.