Increase in pulse wavelength causes the systemic arterial tree to degenerate into a classical windkessel

2007 ◽  
Vol 293 (2) ◽  
pp. H1164-H1171 ◽  
Author(s):  
Mohammad W. Mohiuddin ◽  
Glen A. Laine ◽  
Christopher M. Quick
Keyword(s):  
Heart Rate ◽  
Pulse Pressure ◽  
Systolic Hypertension ◽  
Large Scale ◽  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Arterial System ◽  
System Model ◽  
Isolated Systolic Hypertension ◽  
Arterial Tree

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.

Normalized input impedance and arterial decay time over heart period are independent of animal size

1991 ◽  
Vol 261 (1) ◽  
pp. R126-R133 ◽  
Author(s):  
N. Westerhof ◽  
G. Elzinga
Keyword(s):  
Heart Rate ◽  
Decay Time ◽  
Input Impedance ◽  
Diastolic Pressure ◽  
Arterial Compliance ◽  
Characteristic Impedance ◽  
Peripheral Resistance ◽  
Arterial System ◽  
Heart Period ◽  
Arterial Tree

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)

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
Keyword(s):  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Mean Value ◽  
Pressure Response ◽  
Arterial System ◽  
Response Curves ◽  
Arterial Tree ◽  
Pulse Flow ◽  
Critical Closing Pressure ◽  
Closing Pressure

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.

scholarly journals Increasing pulse wave velocity in a realistic cardiovascular model does not increase pulse pressure with age

2012 ◽  
Vol 303 (1) ◽  
pp. H116-H125 ◽  
Author(s):  
Mohammad W. Mohiuddin ◽  
Ryan J. Rihani ◽  
Glen A. Laine ◽  
Christopher M. Quick
Keyword(s):  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Pressure ◽  
Pulse Wave ◽  
Arterial Compliance ◽  
Arterial System ◽  
System Model ◽  
Transmission Model ◽  
Windkessel Model ◽  
Reflected Wave

The mechanism of the well-documented increase in aortic pulse pressure (PP) with age is disputed. Investigators assuming a classical windkessel model believe that increases in PP arise from decreases in total arterial compliance ( Ctot) and increases in total peripheral resistance ( Rtot) with age. Investigators assuming a more sophisticated pulse transmission model believe PP rises because increases in pulse wave velocity ( cph) make the reflected pressure wave arrive earlier, augmenting systolic pressure. It has recently been shown, however, that increases in cph do not have a commensurate effect on the timing of the reflected wave. We therefore used a validated, large-scale, human arterial system model that includes realistic pulse wave transmission to determine whether increases in cph cause increased PP with age. First, we made the realistic arterial system model age dependent by altering cardiac output (CO), Rtot, Ctot, and cph to mimic the reported changes in these parameters from age 30 to 70. Then, cph was theoretically maintained constant, while Ctot, Rtot, and CO were altered. The predicted increase in PP with age was similar to the observed increase in PP. In a complementary approach, Ctot, Rtot, and CO were theoretically maintained constant, and cph was increased. The predicted increase in PP was negligible. We found that increases in cph have a limited effect on the timing of the reflected wave but cause the system to degenerate into a windkessel. Changes in PP can therefore be attributed to a decrease in Ctot.

Beat-to-beat estimation of peripheral resistance and arterial compliance during pressure transients

1987 ◽  
Vol 252 (6) ◽  
pp. H1275-H1283 ◽  
Author(s):  
G. P. Toorop ◽  
N. Westerhof ◽  
G. Elzinga
Keyword(s):  
Heart Rate ◽  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Estimation Method ◽  
Aortic Pressure ◽  
Autonomous Nervous System ◽  
Mean Flow ◽  
Arterial Tree ◽  
Total Arterial Compliance

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.

scholarly journals Use of angiotensin II receptor blockers alone and in combination with other drugs: a large clinical experience trial

2001 ◽  
Vol 2 (1_suppl) ◽  
pp. S217-S222
Author(s):  
Matthew R Weir ◽  
Rebecca Y Wang
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Systolic Hypertension ◽  
Large Scale ◽  
Candesartan Cilexetil ◽  
Antihypertensive Drugs ◽  
Isolated Systolic Hypertension ◽  
Open Label ◽  
Background Therapy ◽  
Receptor Blockers

Angiotensin II (Ang II) receptor blockers are the newest class of antihypertensive drugs to be developed. No large-scale clinical trials have been performed to evaluate their efficacy alone, or in combination with other drugs. A large-scale, eight week, open-label, non-placebo-controlled, single-arm trial evaluated the efficacy, tolerability and dose-response of candesartan cilexetil, 16—32 mg once-daily, either as monotherapy or as part of combination therapy, in a diverse hypertensive population in actual practice settings. 6465 patients with high blood pressure, of whom 52% were female and 16% African American, with a mean age of 58 years, were included. 5446 patients had essential hypertension and 1014 patients had isolated systolic hypertension. In order to be included in this study, patients had either untreated or uncontrolled hypertension (systolic blood pressure (SBP) 140—179 mmHg and/or diastolic blood pressure (DBP) 90—109 mmHg inclusive at baseline), despite a variety of other antihypertensive drugs. Of the 5156 patients with essential hypertension and at least one post baseline efficacy measurement, the mean pretreatment blood pressure (BP) was 156/97 mmHg. Candesartan cilexetil monotherapy reduced mean SBP/DBP by 18.0/12.2 mmHg. Similarly, in the 964 patients with isolated systolic hypertension and at least one post baseline efficacy measurement, candesartan cilexetil monotherapy reduced SBP/DBP from 158/81 by 16.5/4.5 mmHg. Candesartan cilexetil was similarly effective when employed as add-on therapy. When added to baseline antihypertensive medication in 51% of the patients with essential hypertension not achieving BP control, additional reduction in BP was achieved regardless of the background therapy, including diuretics (17.8/11.7 mmHg) calcium antagonists (16.6/11.2 mmHg), beta-blockers (16.5/10.4 mmHg), angiotensin-converting enzyme inhibitors (ACE-I) (15.3/10.0 mmHg), and alpha blockers (16.4/10.4 mmHg). Likewise, when candesartan cilexetil was used as add-on therapy in patients with isolated systolic hypertension, there was a consistent further reduction of mean SBP/DBP, regardless of the background therapy. Moreover, these monotherapeutic or add-on efficacy benefits were seen regardless of age (<65 or >65 years), gender, or race. Despite the open-label design of the study which enhances efficacy owing to the placebo effect, the Ang II receptor blocker, candesartan cilexetil either alone, or as an add-on therapy, is highly effective for assisting in the control of systolic and diastolic hypertension.

scholarly journals Elevated Pulse Pressure Is Associated With Low Renal Function in Elderly Patients With Isolated Systolic Hypertension

Hypertension ◽  
2005 ◽  
Vol 45 (4) ◽  
pp. 586-591 ◽  
Author(s):  
Jacobien C. Verhave ◽  
Pierre Fesler ◽  
Guilhem du Cailar ◽  
Jean Ribstein ◽  
Michel E. Safar ◽  
...  
Keyword(s):  
Renal Function ◽  
Elderly Patients ◽  
Pulse Pressure ◽  
Systolic Hypertension ◽  
Isolated Systolic Hypertension

Apparent arterial compliance

1998 ◽  
Vol 274 (4) ◽  
pp. H1393-H1403 ◽  
Author(s):  
Christopher M. Quick ◽  
David S. Berger ◽  
Abraham Noordergraaf
Keyword(s):  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Wave ◽  
Arterial Compliance ◽  
Complex Function ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Arterial System ◽  
Lumped Model ◽  
Total Arterial Compliance

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.

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