A square-pulse flow method for measuring characteristics of the arterial bed

1976 ◽  
Vol 40 (3) ◽  
pp. 425-433 ◽  
Author(s):  
M. G. Bottomley ◽  
G. W. Mainwood

A device was designed to provide a “square” pulse of blood flow into the arterial system. Pulses were injected into the carotid artery of the rabbit during transient cardiac arrest. Analysis of pressure response curves generated by the flow provides information as to the state of the arterial tree. With certain assumptions it is possible to estimate from these curves lumped values of peripheral resistance, critical closing pressure, and arterial compliance. In a series of 12 rabbits the mean value of peripheral resistance was found to be 0.21 +/- 0.7 mmHg-ml-1-min and critical closing pressure was estimated to be 23.6 +/- 3.8 mmHg. This method gives two possible values for arterial compliance 0.036 +/- 0.010 and 0.055 +/- 0.010 ml-mm-1 based, respectively, on the rise and decay curves of the pressure response. The theory and limitations of the method are discussed. The use of the method is illustrated in following the response to increased PCO2 and hemorrhage.

1991 ◽  
Vol 261 (1) ◽  
pp. R126-R133 ◽  
Author(s):  
N. Westerhof ◽  
G. Elzinga

The arterial system of mammals in the weight range from 0.6 to 70 kg is characterized by the three-element windkessel, a succinct representation of the arterial tree consisting of the parameters peripheral resistance (Rp), total arterial compliance (C), and aortic characteristic impedance (Zc). The values of these parameters in resting conditions are related to body mass (M). The time constant, or decay time (tau), of the arterial system (defining rate of decay of aortic pressure in diastole), the product of Rp and C, is also evaluated. The dependencies of the heart period (T, inverse of heart rate), and durations of ejection (Ts) and of diastole (Td) in resting conditions are also determined as a function of M. It is found that Rp = Rp0M-0.93; Zc = Zc0M-0.97; and C = C0M+1.23, where Rp0, Zc0, and C0 are proportionality constants. Zc is thus a constant fraction of Rp in all mammals. tau is related to M as tau = tau 0M+0.29; T and Td are related to M as T = T0M+0.27 and Td = Td0M+0.30, where tau 0, T0, and Td0 are proportionality constants. The duration of diastole is thus a constant fraction of T, and the ratios T/tau and Td/tau are independent of M. The findings indicate that arterial input impedance, normalized to aortic Zc and plotted as a function of frequency normalized to heart rate, is similar for all mammals. The finding that the ratio Td/tau is the same in mammals (and Ts/T and stroke volume/M are constant) explains the constancy of pulse pressure (systolic minus diastolic pressure).(ABSTRACT TRUNCATED AT 250 WORDS)


2007 ◽  
Vol 293 (2) ◽  
pp. H1164-H1171 ◽  
Author(s):  
Mohammad W. Mohiuddin ◽  
Glen A. Laine ◽  
Christopher M. Quick

Two competing schools of thought ascribe vascular disease states such as isolated systolic hypertension to fundamentally different arterial system properties. The “windkessel school” describes the arterial system as a compliant chamber that distends and stores blood and relates pulse pressure to total peripheral resistance ( Rtot) and total arterial compliance ( Ctot). Inherent in this description is the assumption that arterial pulse wavelengths are infinite. The “transmission school,” assuming a finite pulse wavelength, describes the arterial system as a network of vessels that transmits pulses and relates pulse pressure to the magnitude, timing, and sites of pulse-wave reflection. We hypothesized that the systemic arterial system, described by the transmission school, degenerates into a windkessel when pulse wavelengths increase sufficiently. Parameters affecting pulse wavelength (i.e., heart rate, arterial compliances, and radii) were systematically altered in a realistic, large-scale, human arterial system model, and the resulting pressures were compared with those assuming a classical (2-element) windkessel with the same Rtot and Ctot. Increasing pulse wavelength as little as 50% (by changing heart rate −33.3%, compliances −55.5%, or radii +50%) caused the distributed arterial system model to degenerate into a classical windkessel ( r2 = 0.99). Model results were validated with analysis of representative human aortic pressure and flow waveforms. Because reported changes in arterial properties with age can markedly increase pulse wavelength, results suggest that isolated systolic hypertension is a manifestation of an arterial system that has degenerated into a windkessel, and thus arterial pressure is a function only of aortic flow, Rtot, and Ctot.


1998 ◽  
Vol 274 (4) ◽  
pp. H1393-H1403 ◽  
Author(s):  
Christopher M. Quick ◽  
David S. Berger ◽  
Abraham Noordergraaf

Recently, there has been renewed interest in estimating total arterial compliance. Because it cannot be measured directly, a lumped model is usually applied to derive compliance from aortic pressure and flow. The archetypical model, the classical two-element windkessel, assumes 1) system linearity and 2) infinite pulse wave velocity. To generalize this model, investigators have added more elements and have incorporated nonlinearities. A different approach is taken here. It is assumed that the arterial system 1) is linear and 2) has finite pulse wave velocity. In doing so, the windkessel is generalized by describing compliance as a complex function of frequency that relates input pressure to volume stored. By applying transmission theory, this relationship is shown to be a function of heart rate, peripheral resistance, and pulse wave reflection. Because this pressure-volume relationship is generally not equal to total arterial compliance, it is termed “apparent compliance.” This new concept forms the natural counterpart to the established concept of apparent pulse wave velocity.


2017 ◽  
Vol 110 (12) ◽  
pp. 659-666 ◽  
Author(s):  
Denis Chemla ◽  
Edmund M.T. Lau ◽  
Philippe Hervé ◽  
Sandrine Millasseau ◽  
Mabrouk Brahimi ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Stéphane Bar ◽  
Maxime Nguyen ◽  
Osama Abou-Arab ◽  
Hervé Dupont ◽  
Belaid Bouhemad ◽  
...  

Introduction: It has been suggested that dynamic arterial elastance (Eadyn) can predict decreases in arterial pressure in response to changing norepinephrine levels. The objective of this study was to determine whether Eadyn is correlated with determinants of the vascular waterfall [critical closing pressure (CCP) and systemic arterial resistance (SARi)] in patients treated with norepinephrine.Materials and Methods: Patients treated with norepinephrine for vasoplegia following cardiac surgery were studied. Vascular and flow parameters were recorded immediately before the norepinephrine infusion and then again once hemodynamic parameters had been stable for 15 min. The primary outcomes were Eadyn and its associations with CCP and SARi. The secondary outcomes were the associations between Eadyn and vascular/flow parameters.Results: At baseline, all patients were hypotensive with Eadyn of 0.93 [0.47;1.27]. Norepinephrine increased the arterial blood pressure, cardiac index, CCP, total peripheral resistance (TPRi), arterial elastance, and ventricular elastance and decreased Eadyn [0.40 (0.30;0.60)] and SARi. Eadyn was significantly associated with arterial compliance (CA), CCP, and TPRi (p < 0.05).Conclusion: In patients with vasoplegic syndrome, Eadyn was correlated with determinants of the vascular waterfall. Eadyn is an easy-to-read functional index of arterial load that can be used to assess the patient’s macro/microcirculatory status.Clinical Trial Registration:ClinicalTrials.gov #NCT03478709.


1989 ◽  
Vol 257 (3) ◽  
pp. H891-H897 ◽  
Author(s):  
B. D. Zuckerman ◽  
H. F. Weisman ◽  
F. C. Yin

Although atherosclerosis significantly alters the structural characteristics of the arterial tree, its effect on arterial impedance, which is a means of quantifying the functional characteristics of the arterial system, has not been characterized. To assess how one type of atherosclerosis affects impedance, we studied arterial impedance in New Zealand White rabbits after 11 wk on a 2% cholesterol diet. From open-chest aortic pressures and flows, impedance data were obtained from spectral analysis of randomly paced and Fourier analysis of nonpaced beats. Compliance was calculated from the low-frequency impedance moduli by assuming a windkessel model for the arterial system. Under base-line conditions, the atherosclerotic impedance phase spectrum in the low-frequency range remained negative for higher values of frequency than in controls. There was no difference between the groups in mean arterial blood pressure, impedance modulus spectrum, characteristic impedance, compliance, or total peripheral resistance. Wave reflections were, however, increased in the atherosclerotic animals. The differences between the two groups in phase and wave reflection were completely abolished after phenylephrine (3 micrograms.kg-1.min-1). Thus this study demonstrates that under base-line conditions atherosclerosis increases wave reflection at the input to the arterial system in the absence of an alteration in global arterial compliance, total peripheral resistance, or mean blood pressure. This increase is presumably secondary to atherosclerotic changes at arterial sites, which produce local impedance mismatching.


1987 ◽  
Vol 252 (6) ◽  
pp. H1275-H1283 ◽  
Author(s):  
G. P. Toorop ◽  
N. Westerhof ◽  
G. Elzinga

We have used a computer-based parameter estimation method to obtain peripheral resistance, total arterial compliance, and characteristic resistance from the measurement of aortic pressure and flow in the open-thorax cat, assuming the three-element windkessel as a model of the systemic arterial tree. The method can be applied on a beat-to-beat basis in the steady state and in transients. We have validated this method by analyzing nonsteady-state data obtained from an electrical analog with fixed values of the resistances and compliance and by showing that the values obtained by this procedure were within 5% of the fixed values of the circuit. Changes in total peripheral resistance and arterial compliance were studied before, during, and after acute heart rate changes in five open-thorax cats with blocked autonomous nervous system. As expected, the peripheral resistance, estimated during the heart rate transient [3.93 +/- 0.94 (SE) kPa X ml-1 X s] was the same as before the transient (3.53 +/- 0.83 kPa X ml-1 X s); total arterial compliances were also identical (0.28 +/- 0.04 vs. 0.27 +/- 0.03 ml/kPa). In six cats without nervous blockade we obtained similar results. Calculation of peripheral resistance during transients from the mean pressure-to-mean flow ratio, i.e., without correction for arterial compliance, suggested changes in resistance values of less than or equal to 57%, which shows that correction is necessary. The findings indicate that peripheral resistance and total arterial compliance can be estimated in vivo on a beat-to-beat basis, even during hemodynamic transients.


1993 ◽  
Vol 264 (5) ◽  
pp. H1560-H1566 ◽  
Author(s):  
I. Shrier ◽  
S. N. Hussain ◽  
S. Magder

Sympathetically mediated changes in blood pressure are thought to occur through changes in arterial resistance (Ra). To test whether the critical closing pressure (Pcrit) could also play a role, we pump-perfused the vascularly isolated canine hindlimb at constant flow. Carotid sinuses were isolated and both vagus nerves cut. Carotid sinus (Pcar), arterial, perfusion (Pper), and venous (Pv) pressures and flow to the hindlimb (Q, electromagnetic flow probe) were measured. By decreasing pump flow to zero over time periods of 1-10 s and measuring the pressure at zero-flow, it was possible to estimate arterial compliance and Pcrit. Ra was calculated as (Pper - Pcrit)/Q. Venous resistance was calculated as (Pel - Pv)/Q, where Pel is the pressure in the compliant region obtained by the double-occlusion technique. Raising Pcar from 115 +/- 7 to 203 +/- 10 mmHg (n = 6) decreased Pcrit from 49.7 +/- 4.3 to 25.9 +/- 2.6 mmHg and Ra from 10.7 +/- 1.2 to 6.8 +/- 0.9 mmHg.min.100 g-1.ml-1 (P < 0.05). Lowering Pcar from 119 +/- 6 to 71 +/- 6 mmHg (n = 6) increased Pcrit from 37.0 +/- 3.3 to 61.0 +/- 8.5 mmHg and Ra from 10.0 +/- 1.6 to 14.0 +/- 2.4 mmHg.min.100 g.ml-1 (P < 0.05). Arterial compliance increased when Pcar was raised (P < 0.05) and decreased when Pcar was decreased (P < 0.1). Venous resistance did not change when Pcar was altered. In conclusion, changes in carotid sinus stimulation alters blood flow to the hindlimb through changes in both Pcrit and Ra.


1985 ◽  
Vol 63 (9) ◽  
pp. 1057-1064
Author(s):  
B. Lowell Langille ◽  
Catherine Osberg

Pressure transients resulting from square-wave changes in abdominal aortic blood flow rate were used to derive effective arterial compliance and peripheral resistance of the hind-limb circulation of anaesthetized rabbits. The model for deriving these parameters proved applicable if step changes in flow were kept less than 35% of mean flow. Under resting conditions, the effective hind-limb arterial compliance of normal rabbits averaged 3.46 × 10−3 mL/mmHg (1 mmHg = 133.322 Pa). Hind-limb arterial compliance decreased with increasing pressure at low arterial pressures, but unlike compliance of isolated arterial segments, compliance did not vary at and above normal resting pressures. Baroreflex destimulation (bilateral carotid artery occlusion) caused an increase in effective hind-limb vascular resistance at 48.4% and a decrease of arterial compliance of 50.7%, so that the constant for flow-induced arterial pressure changes (resistance times compliance) was largely unchanged. Similarly, the arterial time constant for rabbits with chronic hypertension was similar to that for controls because threefold increases in hind-limb vascular resistance were offset by decreases in compliance. Reflex-induced decreases in arterial compliance are probably mediated by sympathetic nerves, whereas decreases associated with hypertension are related to wall hypertrophy in conjunction with increased vasomotor tone. Arterial compliance decreased with increasing pressure in hypertensive animals, but this effect was less pronounced than in normotensive rabbits.


2002 ◽  
Vol 282 (3) ◽  
pp. H1041-H1046 ◽  
Author(s):  
Patrick Segers ◽  
Nikos Stergiopulos ◽  
Nico Westerhof

Effective arterial elastance ( E a), defined as the ratio of left ventricular (LV) end-systolic pressure and stroke volume, lumps the steady and pulsatile components of the arterial load in a concise way. Combined with E max, the slope of the LV end-systolic pressure-volume relation, E a/ E max has been used to assess heart-arterial coupling. A mathematical heart-arterial interaction model was used to study the effects of changes in peripheral resistance ( R; 0.6–1.8 mmHg · ml−1 · s) and total arterial compliance (C; 0.5–2.0 ml/mmHg) covering the human pathophysiological range. E a, E a/ E max, LV stroke work, and hydraulic power were calculated for all conditions. Multiple-linear regression analysis revealed a linear relation between E a, R/ T (where T is cycle length), and 1/C: E a= −0.13 + 1.02 R/ T + 0.31/C, indicating that R/ T contributes about three times more to E a than arterial stiffness (1/C). It is demonstrated that different pathophysiological combinations of R and C may lead to the same E a and E a/ E max but can result in differences of 10% in stroke work and 50% in maximal power.


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