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Arterial Flow

PanVascular Medicine

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Abstract

Arterial flow is a three-dimensional unsteady process that is analyzed by measurements as well as physiological, biological, and mechanical experiments and numerical simulations. Few quantities can be noninvasively measured; they encompass cardiac frequency and peripheral arterial blood pressure as well as velocity and flow rate in given arterial stations by functional imaging. The central arterial blood pressure, from which clinicians derive several indices that are related to the physiological state of compartments of the cardiovascular apparatus, is measured using catheter-based transducers. Research is carried out to adequately infer the aortic pressure from measures in peripheral arteries using efficient signal processing.

Blood flows through deformable arteries that dilate and constrict. Expansion of elastic arteries (Windkessel effect) that constitute the upstream compartment of the arterial tree transforms the systolic bolus into a pulsatile flow. Furthermore, the perfusion of the cardiac pump by coronary arteries benefits from the backflow generated by the wall recoil in elastic arteries. However, the arterial deformation is not only passive but also active. Mural cells sense and react to the stress field and adjust the caliber of the arterial lumen accordingly using intra-, auto-, juxta-, and paracrine signaling. The arterial wall is innervated and perfused from the lumen and vasa vasorum, hence receiving nervous and endocrine cues that are transduced for appropriate outputs. The vasomotor tone determines the level of the flow resistance.

Regulation of the arterial flow has been widely investigated by physiologists, exhibiting the intricated and complex mechanisms that control the body’s homeostasis and adapt the local blood supply to the needs. At lower length scales, biologists describe the entire set of regulators and demonstrate their respective role and the functioning of signaling pathways in normal and pathological conditions. Biomechanicians develop new methods to assess the rheology and behavior of living tissues and, in collaboration with applied mathematicians, model physiological and pathophysiological processes. Some mechanical aspects that are easily handled in mechanics (e.g., applied to civil engineering and aeronautics) cannot be directly used in biomechanics. First, the architecture and the structure are much more complicated. Second, blood is carried in arterial lumens surrounded by three-layered walls made of composite materials. Both blood and wall are biological tissues, water being a major component. Hence, the fluid–structure interaction problem requires specific numerical treatment and elaboration of proper algorithms and multiphysics coupling softwares. Numerical tests are nevertheless carried out using simplifying assumptions and can be useful in medical practice.

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Notes

  1. 1.

    Regulator of the pattern of tissue development during morphogenesis.

  2. 2.

    β-Adrenoceptors are the predominant subtype in skeletal muscle, mostly of the β2 subtype (7–10 % 1-adrenoceptors) (Lynch and Ryall 2008). However, α-adrenoceptors reside in skeletal muscles; they are expressed in higher proportions in highly vascularized muscles (Lynch and Ryall 2008).

  3. 3.

    The Gq/11-coupled α1-adrenoceptors cause vasoconstriction of large resistance arterioles and support cardiac adaptation to stress. In fact, sympathetic vasoconstriction of large resistance arterioles is induced by both α1- and α2-adrenoceptors.

Abbreviations

Augmentation index (AIx):

Quantity derived from the ascending aortic pressure waveform that is the difference between the first (inflection point of the pressure ramp) and second (true) systolic pressure peaks expressed as a percentage of the pulse pressure.

Diastolic arterial blood pressure (DBP):

Minimal pressure value that is an index of the peripheral vessel state, that is, systemic vascular resistance, for a given blood flow rate, as it can be associated with the incident pressure wave.

Diastolic pressure time interval (DPTI):

Time from the dicrotic notch of the aortic pressure wave to the end of the waveform.

Mean arterial pressure (MAP):

Pressure of the steady component of the blood pressure. It depends on time-average values of stroke volume (left ventricular contractility) and cardiac frequency, on the one hand, as well as vascular impedance (resistance and compliance) on the other.

The mean arterial pressure can be considered in a first approximation as the CO × SVR product. The mean arterial pressure is currently estimated by

$$ {p}_{\mathrm{d}}=\left({p}_{\mathrm{s}}-{p}_{\mathrm{d}}\right)/3. $$
(1)

In fact, the mean arterial pressure is underestimated using 0.333 as a multiplier rather than 0.412 (Meaney et al. 2000):

$$ \mathrm{mAP}={p}_{\mathrm{d}}+0.412\left({p}_{\mathrm{s}}-{p}_{\mathrm{d}}\right). $$
(2)
Pulse pressure (PP):

Difference between the systolic (SBP or p s) and diastolic (DBP or p d) arterial blood pressure. It depends on the stroke volume and the impedance (compliance and resistance) of the arterial bed. It is mainly proportional to stroke volume and inversely proportional to arterial compliance.

Subendocardial viability ratio (SEVR):

DPTI/SPTI ratio.

Systolic arterial blood pressure (SBP):

Peak pressure (maximum of the pressure waveform) that reflects the cardiac output and distensibility of elastic arteries (Windkessel effect), as it is set by the reflected pressure wave.

Systolic pressure time interval (SPTI):

Time from the foot of the aortic pressure wave to the dicrotic notch.

Time to wave reflection (TR):

Time from the foot of the aortic pressure wave to the inflection point of the accelerating phase (first systolic peak).

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  1. Team INRIA-UPMC-CNRS REO, Laboratoire Jaques-Louis Lions, CNRS UMR 7598, University Pierre and Marie Curie, Paris, F-75252, Cedex 05, France

    Marc Thiriet

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    Peter Lanzer

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Thiriet, M. (2014). Arterial Flow. In: Lanzer, P. (eds) PanVascular Medicine. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-37393-0_26-1

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    Physiology and Pathophysiology of Arterial Flow
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    03 June 2014

    DOI: https://doi.org/10.1007/978-3-642-37393-0_26-2

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    Arterial Flow
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    DOI: https://doi.org/10.1007/978-3-642-37393-0_26-1

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