True Arterial System Compliance Estimated From Apparent Arterial Compliance

Quick, Christopher M.; Berger, David S.; Hettrick, Douglas A.; Noordergraaf, Abraham

doi:10.1114/1.268

Cited by 35 publications

(32 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although a simple Windkessel model cannot account for wave travel in itself, the energy contacts between all the elements in this expanded model representation of the arterial system can account for distortions in the arterial waveform produced by wave reflection, interpreting these changes in terms of the capacitive, inertial and resistance elements in the system. Indeed, the increasing blood pressure and decreasing heart rate observed with the incremental infusion of L-NAME creates a situation whereby the arterial system degenerates to a Windkessel [30]. While other methods of waveform analysis and interpretation may be applicable in describing the haemodynamic consequences of nitric oxide manipulation of arterial tone in humans, the present model-based interpretations appear physiologically sound.…”

Section: Discussionmentioning

confidence: 90%

Nitric oxide modulation of blood vessel tone identified by arterial waveform analysis

McVeigh¹,

ALLEN²,

MORGAN³

et al. 2001

Clinical Science

View full text Add to dashboard Cite

Traditionally, nitric oxide-mediated alteration in blood vessel tone has been inferred from changes in flow in response to physical and pharmacological interventions using plethysmographic or ultrasonic techniques. We hypothesized that alteration in pulsatile arterial function may represent a more sensitive measure to detect and monitor nitric oxide-mediated modulation of arterial smooth muscle tone. Healthy male volunteers (n = 15) had radial artery pressure pulse waveforms recorded using a calibrated tonometer device. A computer-based assessment of the diastolic pressure decay was employed to quantify changes in arterial waveform morphology in terms of altered pulsatile (arterial compliance) and steady-state (peripheral resistance) haemodynamics. N(G)-nitro-L-arginine methyl ester (L-NAME), a stereospecific inhibitor of nitric oxide synthesis, was infused intravenously in incrementally increasing doses of 0.25, 0.5 and 0.75 mg/kg for 8 min each. Subjects then received either L-arginine or D-arginine (200 mg/kg over 15 min) intravenously in a blinded fashion. On a separate day, subjects had radial artery pressure pulse waveforms recorded before and after the sublingual administration of glyceryl trinitrate, an exogenous donor of nitric oxide. Cardiac output and heart rate decreased and mean arterial blood pressure increased significantly (P < 0.01 for all) in response to the incremental intravenous infusion of L-NAME. Small artery compliance decreased, whereas systemic vascular resistance increased in response to nitric oxide synthesis inhibition (P < 0.01 for both). The intravenous infusion of L-arginine restored the pulsatile and steady-state haemodynamic parameters to pre-treatment values, whereas D-arginine had no effect. Sublingual glyceryl trinitrate decreased systemic vascular resistance by 11%, whereas large artery- and small artery-compliance increased by 25% and 44% respectively. Pressure pulse contour analysis represents a sensitive and convenient technique capable of tracking changes in the pulsatile function of arteries accompanying nitric oxide-mediated alteration in arterial smooth muscle tone.

show abstract

Section: Discussionmentioning

confidence: 90%

Nitric oxide modulation of blood vessel tone identified by arterial waveform analysis

McVeigh¹,

ALLEN²,

MORGAN³

et al. 2001

Clinical Science

View full text Add to dashboard Cite

show abstract

“…The idea here of analyzing beat-to-beat ABP variability in order to circumvent confounding wave phenomena is supported by a previous technique introduced by Quick et al [24]. These investigators extended the standard Windkessel theory (Fig.…”

Section: Discussionmentioning

confidence: 55%

Continuous Cardiac Output Monitoring by Peripheral Blood Pressure Waveform Analysis

Mukkamala

Reisner

Hojman

et al. 2006

IEEE Trans. Biomed. Eng.

107

View full text Add to dashboard Cite

Abstract-A clinical method for monitoring cardiac output (CO) should be continuous, minimally invasive, and accurate. However, none of the conventional CO measurement methods possess all of these characteristics. On the other hand, peripheral arterial blood pressure (ABP) may be measured reliably and continuously with little or no invasiveness. We have developed a novel technique for continuously monitoring changes in CO by mathematical analysis of a peripheral ABP waveform. In contrast to the previous techniques, our technique analyzes the ABP waveform over time scales greater than a cardiac cycle in which the confounding effects of complex wave reflections are attenuated. The technique specifically analyzes 6-min intervals of ABP to estimate the pure exponential pressure decay that would eventually result if pulsatile activity abruptly ceased (i.e., after the high frequency wave reflections vanish). The technique then determines the time constant of this exponential decay, which equals the product of the total peripheral resistance and the nearly constant arterial compliance, and computes proportional CO via Ohm's law. To validate the technique, we performed six acute swine experiments in which peripheral ABP waveforms and aortic flow probe CO were simultaneously measured over a wide physiologic range. We report an overall CO error of 14.6%.

show abstract

“…On the other hand, with a CVP measurement, direct estimation of the cardiopulmonary TPR baroreflex impulse response is, in principle, feasible. In addition, Quick et al (23) proposed to estimate AC by likewise exploiting slow, beat-to-beat fluctuations in ABP and CO via the calculated impedance of the SAT (23). The extended technique here is different in that it attempts to be more precise by also accounting for baroreflex dynamics.…”

Section: Discussionmentioning

confidence: 99%

Estimation of the total peripheral resistance baroreflex impulse response from spontaneous hemodynamic variability

Chen

Kim²,

Sala‐Mercado³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

DS, Mukkamala R. Estimation of the total peripheral resistance baroreflex impulse response from spontaneous hemodynamic variability. Am J Physiol Heart Circ Physiol 294: H293-H301, 2008. First published November 2, 2007 doi:10.1152/ajpheart.00852.2007.-We previously developed a mathematical analysis technique for estimating the static gain values of the arterial total peripheral resistance (TPR) baroreflex (GA) and the cardiopulmonary TPR baroreflex (GC) from small, spontaneous beat-to-beat fluctuations in arterial blood pressure, cardiac output, and stroke volume. Here, we extended the mathematical analysis so as to also estimate the entire arterial TPR baroreflex impulse response [hA(t)] as well as the lumped arterial compliance (AC). The extended technique may therefore provide a linear dynamic characterization of TPR baroreflex systems during normal physiological conditions from potentially noninvasive measurements. We theoretically evaluated the technique with respect to realistic spontaneous hemodynamic variability generated by a cardiovascular simulator with known system properties. Our results showed that the technique reliably estimated hA(t) [error ϭ 30.2 Ϯ 2.6% for the square root of energy (EA), 19.7 Ϯ 1.6% for absolute peak amplitude (PA), 37.3 Ϯ 2.5% for GA, and 33.1 Ϯ 4.9% for the overall time constant] and AC (error ϭ 17.6 Ϯ 4.2%) under various simulator parameter values and reliably tracked changes in GC. We also experimentally evaluated the technique with respect to spontaneous hemodynamic variability measured from seven conscious dogs before and after chronic arterial baroreceptor denervation. Our results showed that the technique correctly predicted the abolishment of hA (t) , and GA ϭ Ϫ2.1 Ϯ 0.6 to 0.3 Ϯ 0.2 (P Ͻ 0.05)] and the enhancement of GC [Ϫ0.7 Ϯ 0.44 to Ϫ1.8 Ϯ 0.2 (P Ͻ 0.05)] following the chronic intervention. Moreover, the technique yielded estimates whose values were consistent with those reported with more invasive and/or experimentally difficult methods. autonomic nervous system; hemodynamics; modeling; system identification; transfer function THE TOTAL PERIPHERAL RESISTANCE (TPR) baroreflex is a wellappreciated feedback control mechanism for rapid arterial blood pressure (ABP) regulation. Consistent with negative feedback, the arterial TPR baroreflex is widely known to respond to a step increase (decrease) in ABP by decreasing (increasing) steady-state TPR. Similarly, the cardiopulmonary TPR baroreflex has been shown to respond to a step increase (decrease) in central venous pressure (CVP) by decreasing (increasing) steady-state TPR (24). In this way, the cardiopulmonary TPR baroreflex is able to anticipate and thereby quickly buffer the imminent change in ABP that will arise from the preload alteration.Much of our knowledge of the TPR baroreflex systems is owed to open-loop studies in which the steady-state or static gain properties of one baroreflex was experimentally determined by selectively exciting it and measuring the steady-state TPR response via Ohm's law [i.e., ABP ...

show abstract

True Arterial System Compliance Estimated From Apparent Arterial Compliance

Cited by 35 publications

References 22 publications

Nitric oxide modulation of blood vessel tone identified by arterial waveform analysis

Nitric oxide modulation of blood vessel tone identified by arterial waveform analysis

Continuous Cardiac Output Monitoring by Peripheral Blood Pressure Waveform Analysis

Estimation of the total peripheral resistance baroreflex impulse response from spontaneous hemodynamic variability

Contact Info

Product

Resources

About