Carotid Artery Waveforms Research Articles

Proof-of-concept for a non-invasive, portable, and wireless device for cardiovascular monitoring in pediatric patients.

Measurement of cardiac function is vital for the health of pediatric patients with heart disease. Standard tools to measure function including echocardiogram and magnetic residence imaging are time intensive, costly, and have limited accessibility. The Vivio is a novel, non-invasive, handheld device that screens for cardiac dysfunction by analyzing intrinsic frequencies (IF) ω1 and ω2 of carotid artery waveforms. Prior studies demonstrated that left ventricular ejection fraction can be derived from IFs in adults. This study 1) studies whether the Vivio can capture carotid arterial pulse waveform data in children ages 0-19 years old; 2) tests the performance of two sensor head geometries, one larger and smaller than the standard size used in adults, designed for the pediatric population; 3) compares the IFs between pediatric age groups and adults with normal function. The Vivio successfully measured a carotid artery waveform in all children over 5 years old and 28% of children under the age of five. The small head did not accurately measure a waveform in any age group. One-way analysis of variance (ANOVA) demonstrated a difference in the IF ω1 between the adult and pediatric cohorts (F = 7.3, Prob>F = 0.0001). Post host analysis demonstrated a difference between the adult cohort (ω1 = 99 +/- 5 bpm) and the cohorts ages 0-4 (ω1 = 111 +/- 2 bpm; p = 0.0006) and 15-19 years old (ω1 = 105 +/-5 bpm; p = 0.02). One-way ANOVA demonstrated a difference in the IF ω2 between the adult and pediatric cohorts (F = 4.8, Prob>F = 0.003), specifically between the adult (ω2 = 81 +/- 13 bpm) and age 0-4 cohorts (ω2 = 48 +/- 8 bpm; p = 0.002). These results suggest that the Vivio can be used to capture carotid pulse waveform data in pediatric populations and that the data produced can be used to measure intrinsic frequencies.

The Lone Carotid: Ultrasound Findings in Rare Innominate Artery Occlusion

A 70-year-old woman presented with bilateral asymptomatic carotid bruits. Carotid duplex ultrasound demonstrated to-and-fro right carotid artery waveforms, retrograde right vertebral artery flow, and monophasic waveforms in the right subclavian artery. This triad of findings indicates significant stenosis or occlusion of the innominate artery. Computed tomography angiography showed an occluded innominate artery, as well as an occluded left proximal vertebral artery, resulting in the left carotid artery being the only direct source of blood flow to the brain and right upper extremity via a patent Circle of Willis. Significant innominate artery blockage is an infrequent finding and, as such, publications regarding its prevalence, treatment, and natural course are scant. We report an unusual case of an innominate artery obstruction.

Association of common carotid artery Doppler-determined dicrotic notch velocity with the left ventricular ejection fraction.

The appearance of the dicrotic notch on blood pressure tracings is associated with impaired cardiac function. Common carotid artery waveforms have similar fiduciary markers, yet they have not been related to cardiac function. We studied associations of common carotid artery dicrotic notch velocities with the left ventricular ejection fraction (LVEF) determined by echocardiography. We conducted a retrospective study of 37 patients who had cardiac echocardiography and carotid Doppler evaluations within 1 day of each other. The LVEF was determined by the biplane modified Simpson rule. Doppler parameters were measured from tracings of the left common carotid artery 4 cm from the flow divider. Linear regression and stepwise multivariable linear regression models were used to evaluate any association between the LVEF and the following variables: age, sex, peak systolic velocity (PSV), end-diastolic velocity (EDV), dicrotic notch velocity, rise time (EDV to PSV), resistive index, and cardiac cycle length. The dicrotic notch velocity was the only variable associated with the LVEF (P = .028) in a bivariate analyses. A backward selection stepwise multivariable equation predicting the LVEF had the dicrotic notch (P = .001) and resistive index (P = .01) as significant predictors, whereas the cardiac cycle length (P = .08) and PSV (P = .08) were borderline not significant. Model goodness of fit was R(2) = 0.37 (P = .004). Dicrotic notch velocities measured from common carotid artery Doppler waveforms are associated with the LVEF and might offer some clinical value in selected cases.

Is a Low End-Diastolic Velocity Parameter Enough to Exclude an 80–99% Internal Carotid Artery Stenosis?

Introduction —High resistive internal carotid artery (ICA) waveforms (high peak systolic velocity >250 cm/sec with low end-diastolic velocity (EDV) <125 cm/sec, having an external carotid artery waveform appearance) are uncommon and present a diagnostic challenge for intervention. Most ICA stenotic classifications rely on a greater EDV to delineate a critical stenosis of 80–99%. Methods —Review of a multiple-laboratory, single-center, Intersocietal Accreditation Commission-accredited, noninvasive vascular laboratory database for ICA carotid examinations performed from January 1, 2008 to November 1, 2012, with a positive stenotic range >60%. Medical records, archived ultrasound images, and correlative imaging studies were reviewed. Results —A total of 843 carotid duplex studies (1,686 arteries) positive for >60% stenoses of at least one side were reviewed. There were 102 duplex studies with high resistive ICA waveforms that were identified. Of these, 35 duplex studies had 40 correlative results, and 67 duplex studies did not have any correlative results. Of the 35 correlated duplex studies, median age was 78 years (range, 53–86 years). Gender distribution was 57% male. The median age of the male subjects was 77 years with a range of 63–82 years and the median age of female subjects was 73 years old with a range of 53–86 years. Seven of the 35 patients presented with symptoms of visual disturbance, transient ischemic attack, or syncope (21% symptomatic). Side distribution was 12 males and 8 females had right-side involvement, and 7 males and 7 females had left-side involvement. There was one female patient who had bilateral involvement. This provides us with 36 duplex ultrasound studies to correlate. Mean PSV was 369 cm/sec (range, 187–492 cm/sec). Mean EDV was 89 cm/sec (range 18–130 cm/sec). Average ICA/common carotid artery ratio was 6.2 (range, 3.2–12.5). Correlative computed tomography angiography was available for 12 of the studies, angiography for 10 of the studies, and surgical findings for 18 of the 35 studies. Conclusion —Assessing all Doppler parameter used to categorize an ICA stenotic range may be beneficial in determining the need for patient intervention. Sonographer impression of audible clues and cardiac history is helpful to the interpreting physician reviewing 2D images and waveforms.

Secondary flow structures under stent-induced perturbations for cardiovascular flow in a curved artery model

Secondary flows within curved arteries with unsteady forcing result from amplified centrifugal instabilities and are expected to be driven by the rapid accelerations and decelerations inherent in physiological waveforms. These secondary flows may also affect the function of curved arteries through pro-atherogenic wall shear stresses, platelet residence time and other vascular response mechanisms.Planar PIV measurements were performed under multi-harmonic non-zero-mean and physiological carotid artery waveforms at various locations in a rigid bent-pipe curved artery model. Results revealed symmetric counter-rotating vortex pairs that developed during the acceleration phases of both multi-harmonic and physiological waveforms. An idealized stent model was placed upstream of the bend, which initiated flow perturbations under physiological inflow conditions. Changes in the secondary flow structures were observed during the systolic deceleration phase (t/T≈0.20–0.50). Proper Orthogonal Decomposition (POD) analysis of the flow morphologies under unsteady conditions indicated similarities in the coherent secondary-flow structures and correlation with phase-averaged velocity fields.A regime map was created that characterizes the kaleidoscope of vortical secondary flows with multiple vortex pairs and interesting secondary flow morphologies. This regime map in the curved artery model was created by plotting the secondary Reynolds number against another dimensionless acceleration-based parameter marking numbered regions of vortex pairs.

Noninvasive assessment of central and peripheral arterial pressure (waveforms): implications of calibration methods

Noninvasive estimation of central blood pressure (BP) from radial artery pressure waveforms is increasingly applied. We investigated the impact of radial artery waveform calibration on central BP assessment and calculated pressure amplification, with focus on the one-third rule used to estimate mean arterial BP (MAP). Pressure waveforms were noninvasively measured at the radial and carotid arteries in 1873 individuals (age 45.8+/-6.1 years). Radial and carotid artery waveforms were calibrated using brachial artery DBP and SBP, MAP estimated with the one-third rule and MAP estimated as brachial DBP along with 40% of brachial artery pulse pressure. Central SBP obtained via a transfer function was 123.5 +/- 15.7, 117.8 +/- 14.2 and 126.0 +/- 15.4 mmHg (mean +/- SD) following above-mentioned three calibration schemes, respectively. Using the same calibration schemes, carotid artery SBP was 131.4 +/- 15.2, 118.4 +/- 14.4 and 126.8 +/- 15.7 mmHg, respectively. Central-to-brachial amplification was 13.0 +/- 3.6 mmHg using second method as compared with 4.6 +/- 3.8 mmHg with third method. Brachial-to-radial amplification was actually negative (-6.3 +/- 4.5 mmHg) using second method, whereas 3.4 +/- 5.5 mmHg was found with third method. Both carotid artery SBP and central SBP obtained via a transfer function are highly sensitive to the calibration of the respective carotid artery and radial artery pressure waveforms. Our data suggest that the one-third rule to calculate MAP from brachial cuff BP should be avoided, especially when used to calibrate radial artery pressure waveforms for subsequent application of a pressure transfer function. Until more precise estimation methods become available, it is advisable to use 40% of brachial pulse pressure instead of 33% to assess MAP.

Abstract 4962: Influence of Adiposity on Carotid Wave Reflection and Arterial Stiffness: A Longitudinal Study in Healthy Children

Background: The relationship between childhood obesity and adverse cardiovascular outcomes during adulthood may be mediated through the promotion of impaired vascular function. Wave reflection is an index of arterial function that is determined by arterial stiffness and is predictive of adverse cardiovascular events in adults. We hypothesized that baseline and changes in adiposity during childhood have an adverse influence on future levels of wave reflection and arterial stiffness. Methods: In 514 healthy children (mean age 8.3±0.4, 50% boys); percentage body fat (%BF) was quantitated by dual-energy x-ray absorptiometry during a baseline assessment in 2005 and during a follow-up assessment in 2007. Baseline insulin resistance was evaluated using a homeostasis model assessment (HOMA-IR). Cardiorespiratory fitness (CRF) was assessed using a 20 meter shuttle run. Carotid artery wave reflection and carotid-femoral pulse wave velocity (PWV) was assessed in 2007 using applanation tonometry (SphygmoCor, Atcor Medical, Sydney, Australia). The second peak of carotid systolic blood pressure (SBP2) was obtained from the carotid arterial waveform. Results: In univariable analysis, baseline %BF was positively associated with carotid SBP2 and PWV measured in 2007. In multivariable analysis, baseline %BF and change in %BF was associated with carotid SBP2 after adjustment for age, sex, baseline blood pressure, heart rate, height, HOMA-IR, total cholesterol and CRF (Table ). Baseline %BF was also independently associated with PWV (Table ). Conclusion: Baseline adiposity was positively related to future carotid wave reflection and arterial stiffness. In addition, subsequent increase in adiposity over a 2-year period was associated a greater degree of wave reflection. Relationship between baseline and change in percent body fat and future wave reflection (carotid SBP2) and arterial stiffness (PWV) in multivariate models

Pathogenesis of Elevated Peripheral Pulse Pressure

“Ashes to ashes, dust to dust, if the cancer don’t get us, the arteriosclerosis must” — —Richard Gordon in The Alarming History of Medicine, 1993 Substantial evidence suggests that arterial remodeling evolves over a life course under the conjoint influence of genes, environmental factors (including vascular risk factors), and lifestyle characteristics (such as diet and physical activity).1 Such arterial remodeling involves multiple vascular territories and is panarterial, ie, it involves all layers of the arterial wall.1 More recently, considerable attention has focused on the physiological aspects of propagation of blood within the aorta, and several important concepts have evolved. First, the aorta is no longer regarded as just a passive conduit that transports blood to the vital organs. Rather, it is a complex organ that remodels in dynamic fashion in response to biomechanical stresses that accumulate over the life course.1 The different segments of the aorta vary in their relations to risk factors, underscoring the heterogeneity in remodeling characteristics across the arterial tree.2 Second, age-associated changes in the aortic wall include fragmentation of the elastin fibers, increased synthesis of collagen, and calcification. The molecular epidemiology of these vascular remodeling changes have been well characterized, and are complex, being mediated via the interaction of vascular smooth muscle cells, integrins, metalloproteinases, endothelial function, and the renin-angiotensin axis, inflammation, and other pathways.1 Third, vascular flow propagation is the combination of steady flow (mean arterial pressure) and pulsatile (pulse pressure) components. The proximal (central) aorta stiffens with age, and these changes are associated with an increase in the pulsatile component (increased central pulse pressure), which in turn places a burden of increased afterload on the left ventricle. There is widespread agreement that elevated pulsatile load is associated with increased risk of cardiovascular disease, including myocardial infarction, stroke, and heart …

Pulsology Reloaded

The Losartan Intervention For Endpoint reduction in hypertension (LIFE) Study,1 the Second Australian National Blood Pressure Trial (ANBP2),2 and the Anglo-Scandinavian Cardiovascular Outcome Trials3 have shown that different antihypertensive treatments may have different impacts on the rate of events in hypertension while achieving comparable brachial blood pressure (BP) reduction. Thus, although brachial BP estimation by classic Riva–Rocci cuff sphygmomanometer and the Korotkoff auscultatory technique have provided almost all of our knowledge on epidemiology, prognosis, and treatment of hypertension,4,5 recent trials1–3 are revealing intrinsic limitations of the conventional approach, because the real goal of treatment in hypertension is the reduction in the number and the rate of untoward events. More recently, the Conduit Artery Function Evaluation (CAFE) Study6 described higher central BP as a key factor explaining the greater number and rate of events with atenolol than with amlodipine plus perindopril. Central pressure waveform and BP values can be estimated by applanation tonometry, a method supported by solid theoretical principles and modeling studies in experimental settings.7 Analysis of the systolic portion of the carotid pressure waveform allows for obtaining indices of the arterial viscous-elastic properties that correlate with end-organ damage and clinical outcomes in hypertension.8 Therefore, the indices of arterial waveform reflection and mechanics and central BP assessed by applanation tonometry have the potential to add significant information for risk stratification beyond and above brachial BP. In fact, the conclusions of the CAFE Study were well received.9 In addition, applanation tonometry has also been associated with 2D-guided M-mode vascular ultrasonography to assess simultaneously the viscous-elastic properties of the carotid artery, the intima–media thickness, and quantification of atherosclerosis.8 Assessment of cardiovascular target organ damage is curial for a global risk assessment …

Brachial Blood Pressure But Not Carotid Arterial Waveforms Predict Cardiovascular Events in Elderly Female Hypertensives

Central arterial waveforms and related indices of large artery properties can be determined with relative ease. This would make them an attractive adjunct in the risk stratification for cardiovascular disease. Although they have been associated with some classical risk factors and the presence of coronary disease, their prospective value in predicting cardiovascular outcomes is unknown. The present study determined the relative predictive value for cardiovascular disease-free survival of large artery properties as compared with noninvasive brachial blood pressure alone in a population of elderly female hypertensive subjects. We measured systemic arterial compliance, central systolic pressure, and carotid augmentation index in a subset of female participants in the Second Australian National Blood Pressure Study (untreated blood pressure 169/88+/-12/8 mm Hg). There were a total of 53 defined events during a median of 4.1 years of follow-up in 484 women with complete measurements. Although baseline blood pressures at the brachial artery predicted cardiovascular disease-free survival (hazard ratio [HR], 2.3; 95% CI, 1.3 to 4.1 for pulse pressure > or =81 versus <81 mm Hg; P=0.01), no such relation was found for carotid augmentation index (HR, 0.80; 95% CI, 0.44 to 1.44; P value not significant) or systemic arterial compliance (HR, 1.25; 95% CI, 0.72 to 2.16; P value not significant). Blood pressure, but not noninvasively measured central arterial waveforms, predict outcome in the older female hypertensive patient. Thus, blood pressure measurement alone is superior to measurement of arterial waveforms in predicting outcome in this group.

Enhanced external counterpulsation does not alter arterial stiffness in patients with angina

Enhanced external counterpulsation (EECP) is a noninvasive treatment for angina that acutely augments diastolic pressure and reduces cardiac afterload. However, the mechanism of the sustained clinical benefit seen with this therapy is not known. The study aimed to determine whether EECP leads to an improvement in arterial stiffness. In all, 22 men and 1 woman with angina (age 63.6 +/- 6.7 years, mean +/- SD) were studied prior to and after 35 h of EECP therapy over 7 weeks. We measured carotid-radial (C-R) pulse wave velocity (PWV), and aortic augmentation index (AI) was derived from radial and carotid artery waveforms using applanation tonometry. Seventeen patients underwent treadmill exercise testing before and after the 7 weeks of EECP. After EECP therapy, despite a significant improvement in treadmill exercise time and a reduction in systolic and diastolic blood pressures, there was no significant change in any arterial stiffness parameters: Mean C-R PWV was 8.4 +/- 0.8 m/s at baseline and 8.0 +/- 1.2 m/s after 7 weeks of EECP, mean change: -0.4, 95% confidence interval (CI): -1.0, + 0.2, p = 0.17. Mean radial-derived AI was 25.7 +/- 10.4% before and 24.6 +/- 10.8% after, mean change: +1.1%, 95% CI: -2.3, +4.5, p = 0.53. Median AI-carotid was 31.5% before and 28.7% after; median change: -0.5, interquartile range: -9.5, +3.5, p = 0.32. Nineteen patients returned for 6-month recordings; neither blood pressure nor arterial stiffness readings were significantly different from baseline. Enhanced external counterpulsation therapy does not significantly alter arterial stiffness. Other than an initial reduction in blood pressure, the sustained clinical benefit seen with this therapy is unlikely to be effected through alterations in arterial wall mechanical properties.

Derivation of the ascending aortic-carotid pressure transfer function with an arterial model.

To devise a method of deriving the ascending aortic pressure waveform from the noninvasively determined carotid arterial waveform, ascending aortic and carotid arterial pressures were recorded in 13 patients aged 58.5 +/- 10.0 (SD) yr. A single viscoelastic tube terminated with a modified windkessel was used to model the carotid arterial system. For each patient the model parameters, characteristic impedance of the tube (Z0), reflection coefficient at the termination (gamma), and time constant of the windkessel (tau), were estimated by minimizing the root-mean-square error between the measured and predicted carotid waveforms, with the ascending aortic pressure waveform as input. The resulting arterial parameters were realistic: Z0 = 729.5 +/- 246.8 dyn.s.cm-3, gamma = 0.75 +/- 0.19, and tau = 0.16 +/- 0.17 s. A generalized model constructed with these mean parameters yielded a smaller error between predicted and measured carotid arterial pressures (3.4 +/- 1.3 mmHg) than between ascending aortic pressure and measured carotid arterial pressure (4.4 +/- 1.6 mmHg, P < 0.01) and also reproduced the carotid wave contour indexed by the ratio of late systolic to early systolic peak amplitude: predicted = 1.26 +/- 0.05 and measured = 1.24 +/- 0.16 vs. aortic = 1.55 +/- 0.19.

Vascular hypertrophy is an early finding in essential hypertension and is related to arterial pressure waveform contour

The effects of hypertension on the arterial vasculature were examined in a study group of 20 patients with newly diagnosed essential hypertension, 18 patients with chronic essential hypertension, and 32 control subjects with normal blood pressure. Left ventricular mass was determined echocardiographically. Carotid artery intimal—medial thickness was measured by means of B-mode ultrasound imaging, and carotid arterial waveforms were obtained by applanation tonometry. Compared with that in control subjects, carotid intimal—medial thickness was increased in patients with chronic hypertension (0.74 ± 0.17 mm vs 0.61 ± 0.15 mm in control subjects; p < 0.01) and in patients with newly diagnosed hypertension (0.66 ± 0.12 mm vs 0.61 ± 0.15 mm in control subjects; p < 0.05). Left ventricular mass was also higher in patients with chronic hypertension than in control subjects but was very similar between control subjects and those with newly diagnosed hypertension. Both the group with early hypertension and the group with chronic hypertension had an increased incidence of early waveform reflection evident on carotid arterial waveform examination. By multiple regression analysis, independent predictors of increased carotid intimal—medial thickness were age, systolic arterial pressure, and Murgo class of arterial waveform. Conduit arterial wall thickening precedes left ventricular remodeling in essential hypertension and is significantly related to the degree of pressure elevation and the arterial waveform contour.

933-92 Carotid Thickening Precedes Ventricular Remodeling in Early Essential Hypertension and is Significantly Related to Early Wave Reflection

Ventricular and vascular remodeling occur early in essential hypertension, develop in parallel and may be influenced by early arterial wave reflection. To further study these relationship we examined 20 newly diagnosed, untreated mild hypertensives, 18 previously treated hypertensives and to 35 age and sex-matched normotensive normal volunteers (N), with both high frequency B-mode imaging of the carotid artery to determine carotid intima-medial thickness (IMT), diameter (CD) and relative thickness (CRWT = 2*IMT/CD) and 2-D guided M-mode echocardiography for determination of LV posterior wall thickness (PWT), end-diastolic diameter (LVEDD), LV relative wall thickness (LVRWT = 2*PWT/LVEDD) and LV mass index (LVMI). Using high-fidelity arterial tonometry the right carotid artery waveform was recorded and classified by measurement of augmentation index as having either a normal early systolic peak (Type C) or abnormal late systolic peak (Type A-indicating early wave reflection). Compared to N, the treated hypertensives had significantly higher LVMI (98 ± 22 vs 82 ± 22 g/m2, p &lt; 0.05) and carotid IMT (0.74 ± 0.17 vs 0.61 ± 0.15, P &lt; 0.05). There were no significant differences in LVwall thickness, relative wall thickness or LV mass index between subjects with Type A and Type C arterial waveforms. In contrast, carotid IMT was significantly increased in patients with Type A arterial waveforms.Empty CellnLVRWTLVMICIMT (mm)CRWTMAP (mmHg)Type A(47)0.38 ± 0.0985 ± 250.69 ± 0.17*0.22 ± 0.04*105 ± 14*Type C(22)0.38 ± 0.1087 ± 180.59 ± 0.090.19 ± 0.0396 ± 14*p &lt; 0.01 vs. Type C p &lt; 0.01 vs. Type C In multivariate analysis, only age (p &lt; 0.05). systolic blood pressure (p &lt; 0.001) and augmentation index (p &lt; 0.05) were independently associated with, CIMT. We conclude that the Type A arterial waveform indicating abnormal early wave reflection coincides with increased mean arterial pressures and with intima-medial thickening in large conduit arteries. These changes precede left ventricular remodeling and left ventricular hypertrophy in mild, essential hypertension.

Noninvasive Measurement of Central Venous Pressure by Neck Inductive Plethysmography

Bedside estimation of the height at which the internal jugular veins collapse, referenced to a standard hemodynamic location, theoretically reflects central venous pressure. This method has never been demonstrated as accurate when compared to invasive CVP measurements because of the great clinical skills and time required to visually identify the internal jugular venous waveform. Since the principles of the bedside method are sound, we utilized them in conjunction with the neck inductive plethysmograph, a device which has the capability of recording internal jugular venous and carotid arterial waveforms. The respiratory distortion of these vascular waveforms was eliminated by employing a digital bandpass filter, making it easy to identify the venous and arterial waveforms on the videoscreen of a personal computer. The upper torso was positioned while observing the videoscreen until the vascular waveform was seen as a mixed arteriovenous waveform, signifying intermittent internal jugular venous collapse. The height of the internal jugular vein above the phlebostatic axis was obtained by external measurement and recorded as CVPni in cm H 2 O. In 43 patients, 86 percent of CVPni (NIP) values fell within 20 percent CVPi (invasive catheter measurements) over a range of CVP from 0 to 19 cm H 2 O. In an additional seven patients, CVPi was greater than the height that the upper torso could be elevated and an arterial waveform could not be obtained. Here, CVPni was recorded as the value at least exceeding the value measured. In two other patients, obstruction of an internal jugular vein gave spuriously low values of CVPni. Our study indicates that this new neck inductive plethysmographic method is accurate compared to invasive catheter measurements of CVP and should serve as a safe, noninvasive alternative in situations where such measurements are required. (Chest 1991; 100:371-75)

Noninvasive Measurement of Central Venous Pressure by Neck Inductive Plethysmography

Bedside estimation of the height at which the internal jugular veins collapse, referenced to a standard hemodynamic location, theoretically reflects central venous pressure. This method has never been demonstrated as accurate when compared to invasive CVP measurements because of the great clinical skills and time required to visually identify the internal jugular venous waveform. Since the principles of the bedside method are sound, we utilized them in conjunction with the neck inductive plethysmograph, a device which has the capability of recording internal jugular venous and carotid arterial waveforms. The respiratory distortion of these vascular waveforms was eliminated by employing a digital bandpass filter, making it easy to identify the venous and arterial waveforms on the videoscreen of a personal computer. The upper torso was positioned while observing the videoscreen until the vascular waveform was seen as a mixed arteriovenous waveform, signifying intermittent internal jugular venous collapse. The height of the internal jugular vein above the phlebostatic axis was obtained by external measurement and recorded as CVPni in cm H2O. In 43 patients, 86 percent of CVPni (NIP) values fell within 20 percent CVPi (invasive catheter measurements) over a range of CVP from 0 to 19 cm H2O. In an additional seven patients, CVPi was greater than the height that the upper torso could be elevated and an arterial waveform could not be obtained. Here, CVPni was recorded as the value at least exceeding the value measured. In two other patients, obstruction of an internal jugular vein gave spuriously low values of CVPni. Our study indicates that this new neck inductive plethysmographic method is accurate compared to invasive catheter measurements of CVP and should serve as a safe, noninvasive alternative in situations where such measurements are required.

Comparison of zero crossing counter to FFT spectrum of ultrasound Doppler

Doppler data were obtained from a normal carotid, popliteal, and radial artery. It was found that the results of a digital zero-crossing counter-mean frequency estimate and the first moment of the FFT (fast-Fourier-transform)-generated spectra were comparable for high signal-to-noise ratio (SNR), as in the case of the carotid arterial waveform. However, the digital zero-crossing with thresholding was a more accurate representation of the expected velocity-vs.-time waveforms in the case of low-SNR Doppler obtained from the popliteal and radial arteries.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>