Arterial Properties and Compliance

The arteries are not rigid pipes: their walls combine elastic fibres, smooth muscle, and collagen so that the large central arteries stretch with each heartbeat and recoil between beats. This compliance, together with the resistance of the smaller arteries, shapes the arterial pressure waveform and converts the heart's pulsatile ejection into steadier flow to the tissues. Arterial compliance and its loss with ageing and disease — arterial stiffening — are central concepts in vascular physiology.

Definition

Arterial compliance is the change in arterial blood volume produced by a given change in pressure; together with peripheral resistance it determines the arterial pressure waveform. Arterial stiffness is the inverse property, the resistance of the wall to distension.

Scope

This topic covers the mechanical and functional properties of the arterial wall: compliance and elastance, the Windkessel buffering role of the elastic arteries, the resistance role of the small muscular arteries, pulse-wave behaviour, and how these properties change with age. It does not cover clinical hypertension management or arterial disease treatment.

Core questions

• How do elastic arteries store and release energy across the cardiac cycle?
• What determines arterial compliance and how is it measured?
• How do the elastic conduit arteries and the small resistance arteries differ in function?
• Why does arterial stiffness increase with age and what are its consequences for pressure?

Key concepts

• Compliance and elastance
• Elastic (conduit) versus muscular (resistance) arteries
• Pulse pressure and pulse-wave velocity
• Pressure-wave reflection
• Arterial stiffening with ageing
• Wall composition: elastin, collagen, smooth muscle

Key theories

Arterial Windkessel

The elastic large arteries act as a pressure reservoir (Windkessel) that is filled during systolic ejection and discharges during diastole; arterial compliance and peripheral resistance together set the diastolic decay of pressure and the magnitude of pulse pressure.

Mechanisms

During systole the heart ejects blood faster than it can drain through the periphery, so the elastic central arteries distend and store part of the stroke volume; their recoil during diastole maintains forward flow and pressure (the Windkessel function; Westerhof et al., 2008). Compliance depends on wall composition: elastin permits low-pressure distension, while collagen recruitment limits over-distension at higher pressures, giving the wall a non-linear pressure-volume relation. The smaller muscular arteries and arterioles contribute relatively little compliance but provide most of the resistance that, with compliance, shapes the pressure waveform (Mulvany & Aalkjaer, 1990). With ageing, elastin fragments and collagen and other wall changes accumulate, stiffening the large arteries, raising pulse-wave velocity, and increasing pulse pressure (Lakatta & Levy, 2003).

Clinical relevance

Arterial stiffness, quantified chiefly by pulse-wave velocity, is a widely used marker of vascular ageing, and its measurement has been standardised by expert consensus (Laurent et al., 2006). This entry explains the underlying physiology and the meaning of such measurements; it is not clinical guidance and does not direct individual diagnosis or treatment.

Evidence & guidelines

An expert consensus document standardised the definitions, measurement, and reporting of arterial stiffness, with carotid-femoral pulse-wave velocity as a reference index (Laurent et al., 2006). The physiological basis rests on the Windkessel framework (Westerhof et al., 2008) and on structural studies of large and small arteries (Mulvany & Aalkjaer, 1990; Lakatta & Levy, 2003).

History

The idea that the elastic arteries cushion pulsatile flow dates to the nineteenth-century Windkessel ('air chamber') analogy and was later expressed in lumped mathematical models that relate compliance and resistance to the pressure waveform (Westerhof et al., 2008). Twentieth-century structural physiology distinguished the elastic conduit arteries from the muscular resistance arteries (Mulvany & Aalkjaer, 1990), and ageing studies established arterial stiffening as a major correlate of cardiovascular risk (Lakatta & Levy, 2003).

Key figures

• Nico Westerhof
• Stephane Laurent
• Michael J. Mulvany
• Edward G. Lakatta

Seminal works

• westerhof-2008
• mulvany-aalkjaer-1990
• lakatta-levy-2003

Frequently asked questions

What is the difference between arterial compliance and arterial stiffness?

They are inverse descriptions of the same wall property: compliance is how much the artery expands for a given rise in pressure, and stiffness is how much it resists that expansion.

Why does arterial stiffness matter for blood pressure?

Stiffer large arteries store less of the stroke volume during systole, so systolic pressure rises and diastolic pressure falls, widening the pulse pressure.