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Interface 1: Arterial Vascular Function

Arterial Vascular Function

The arterial circulation functions as a pulsatile hydraulic system, alternating between energy storage during systole and energy release during diastole.

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Systole:

During ventricular ejection, a small part of the stroke volume immediately flows into the small arteries and arterioles, while the majority distends the elastic walls of the large arteries (notably the aorta). This distension stores potential energy within the arterial system, much like the bellows pump below. In the picture below, the bellows pump pumps water from a reservoir into a pressurized tank that temporarily holds the incoming water before releasing it steadily to a hose.  This system is often referred to as a Windkessel model  (from the German “air chamber”).  

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Similar to the Windkessel model, the aorta’s elastic expansion (synonymous with the pressurized air tank) allows blood to be temporarily stored under pressure, converting the intermittent output of the heart into a smoother, continuous flow through the vascular tree. The amount of energy stored is determined by the arterial compliance (ΔV/ΔP), or how easily the arteries expand with each ejected volume.

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Diastole:

When the heart relaxes, the elastic recoil of these arteries releases the stored energy, pushing blood forward through the peripheral circulation even in the absence of active ventricular contraction. This recoil maintains diastolic flow and tissue perfusion, preventing pressure and flow from rapidly dropping to zero between beats.

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Similar to the Windkessel model, these properties convert the pulsatile ejection from the heart into a steady, continuous pressure and flow, ensuring efficient convective delivery of oxygen and nutrients to the tissues.

The Arterial Pressure Waveform

 

While the Windkessel model provides a conceptual framework for understanding the relationships between pressure and flow in the arterial circulation, it does not fully describe the cardiovascular interactions involved in creating an arterial pressure waveform. An arterial pressure waveform represents the mechanical energy impulse generated by left ventricular (LV) contraction, transmitted through the aortic valve and propagated along the arterial tree as a pressure wave.

Importantly, this pressure (energy) wave travels much faster than the actual flow of blood, as it reflects the transmission of energy through a nearly incompressible fluid rather than the bulk movement of that fluid itself.

The shape and characteristics of the arterial waveform depend on multiple factors, including arterial compliance, peripheral resistance, and wave reflection, each of which modulates how pressure is transmitted and dampened along the vascular pathway.

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Electrical–Mechanical Coupling

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The electrocardiogram (ECG) and the arterial pressure waveform are intimately related, reflecting two sides of the same process:

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  • The ECG records the electrical activation of the myocardium.

  • The arterial waveform records the mechanical consequence of that activation; the generation and transmission of pressure by the contracting ventricle.

 

There is a short but consistent electromechanical delay between the R-wave on the ECG (which marks the onset of ventricular depolarization) and the systolic upstroke of the arterial pressure waveform. This delay, typically around 120–200 milliseconds, represents the time required for:

  1. The myocardium to develop enough tension to open the aortic valve, and,

  2. The resulting pressure pulse to travel through the arterial system to reach the transducer site.​

The Arterial Pressure Waveform and the Cardiac Cycle

The arterial pressure waveform is a direct mechanical reflection of left ventricular ejection and its interaction with the arterial system.

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This classic Wiggers diagram demonstrates how changes in aortic, ventricular, and atrial pressures are coordinated throughout the cardiac cycle.

  • When ventricular pressure rises above atrial pressure, the atrioventricular (AV) valves close, producing the first heart sound (“lub”) and initiating isovolumetric contraction.

  • As ventricular pressure exceeds aortic pressure, the semilunar valves open, marking the beginning of ventricular ejection; this corresponds to the upstroke of the arterial waveform.

  • When the ventricle relaxes and its pressure falls below aortic pressure, the aortic valve closes, generating the second heart sound (“dub”) and creating the small dicrotic notch on the descending limb of the arterial pressure curve.

  • Diastolic pressure then represents the lowest arterial pressure before the next cardiac cycle, while mean arterial pressure (MAP) corresponds to the average perfusion pressure over the entire cycle.

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When isolating a single arterial waveform, the key landmarks (systolic, diastolic, and mean pressure) are highlighted, and the period of ventricular ejection is identified in gray.

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Together, these figures emphasize that the arterial waveform is not just a pressure tracing, but a dynamic signature of ventricular-arterial interaction, linking electrical excitation, mechanical contraction, and vascular properties into one continuous physiological sequence.

Systolic Upstroke

The systolic upstroke represents the initial phase of ventricular ejection, beginning as the aortic valve opens and left ventricular pressure rapidly exceeds aortic pressure.​​

Systolic Upstroke

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  • The slope of the upstroke reflects how quickly pressure rises in the arterial system and is primarily determined by:

    • Left ventricular contractility: greater inotropy produces a steeper, sharper upstroke as blood is ejected more forcefully and rapidly.

    • Aortic valve function: obstruction (e.g., aortic stenosis) blunts the upstroke and delays its peak.

    • Proximal aortic compliance: stiff arteries resist distention, producing a sharper but narrower upstroke, while compliant arteries generate a smoother, rounded ascent.

In essence, the upstroke encodes both ventricular performance and arterial properties, acting as an early mechanical signature of systolic function and vascular health.

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Peak Systolic Pressure

The peak systolic pressure represents the maximum pressure generated during ventricular ejection, marking the point at which the left ventricle transfers the greatest amount of energy to the arterial system.

Peak Systolic Pressure

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Peak Systolic pressure is determined by three main factors:

  1. Ventricular contractility, which defines how forcefully blood is ejected.

  2. Arterial compliance, which dictates how easily the proximal vessels expand to accommodate ejected volume.

  3. Wave reflections, which occur when the forward pressure wave from systolic ejection encounters changes in vessel caliber or stiffness and reflects back toward the heart (due to bifurcations or a tortuous configuration).

When arteries are stiff, atheromatous, or poorly compliant, they cannot expand effectively during systole. This limited distension leads to a higher rise in peak systolic pressure for a same stroke volume. Similarly, when wave reflections return prematurely (as seen in stiff or poorly compliant arteries, a tortuous vascular tree, or high peripheral resistance) the reflected wave adds to the forward wave during late systole, further increasing the measured peak. This phenomenon is known as pressure augmentation, and its magnitude depends on both the timing and amplitude of the reflected wave.

Clinically, an elevated peak systolic pressure reflects impaired arterial buffering capacity. As both arterial compliance and wave reflections are determinants of the vascular afterload a low compliance and increased wave reflections will increase left ventricular wall stress, raise myocardial oxygen demand, and in vulnerable conditions such as aneurysmal disease or recent hemorrhage, can destabilize clots or precipitate rupture.

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Miller RD (ed): Anesthesia, 5th ed. New York, Churchill Livingstone 2000

As arteries stiffen, the pressure waveform changes noticeably.

  • Pulse pressure widens because systolic pressure rises and diastolic pressure falls.

  • Peak pressure occurs later in systole due to the earlier return of reflected waves.

  • Diastolic pressure decays faster because stiff vessels recoil less effectively.

These findings reflect loss of arterial compliance and premature wave reflection, classic features of vascular aging and isolated systolic hypertension.

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Systolic Decline

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Systolic Decline

The systolic decline represents the transition from active ventricular ejection to passive arterial recoil.

The rate of this decline depends on arterial compliance: when vessels are stiff or poorly compliant, the stored energy in the arterial wall dissipates more quickly, resulting in a steeper, more rapid pressure drop.

In contrast, compliant arteries release stored energy gradually, maintaining diastolic pressure and promoting continuous forward flow during diastole. 

Dicrotic Notch

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Dicrotic Notch

Also known as the incisura (Latin for notch), the dicrotic notch is a small deflection that marks the closure of the aortic valve during the transition from systole to diastole. While aortic valve closure initiates the dicrotic notch, its position and shape on the arterial tracing are influenced by wave reflection and vascular properties (see image below).  Remember that the arterial waveform arises from the interaction of forward pressure waves generated by left ventricular ejection and reflected waves moving in the opposite direction within the arterial tree.  As a result, the dicrotic notch reflects both the closure of the aortic valve and the combined effects of forward and backward (reflected) wave propogation (see below image).    

 

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Interestingly, a rightward shift and low or poorly defined dicrotic notch suggests a reduced systemic vascular resistance and/or impaired wave reflection.  This finding can be seen in conditions like severe distributive shock or vasoplegia, where diastolic recoil and arterial tone are diminished.

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When vascular compliance is poor, the dicrotic notch will shift the opporite direction, towards the point of peak systolic pressure.  

Hover to match the arterial waveform with the proper hemodynamic state
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Distributive/Vasoplegic Shock

This arterial pressure waveform illustrates vasoplegia.  In vasoplegia, profound reductions in systemic vascular resistance and increased arterial compliance attenuate pressure wave reflection from the peripheral circulation. As a result, the backward waves that normally interact with the forward ejection wave are delayed and diminished, leading to a dicrotic notch that is shifted to the right and poorly defined. Although aortic valve closure occurs at its usual timing, the lack of effective wave summation within the arterial tree prevents formation of a sharp, distinct notch on the waveform.

Normal Waveform

This arterial pressure waveform demonstrates normal arterial compliance and vascular tone, resulting in balanced interaction between forward pressure waves generated by left ventricular ejection and reflected waves from the peripheral arterial tree. Aortic valve closure initiates the dicrotic notch, which appears at the expected time and is sharply defined due to appropriate wave reflection and summation. The position and clarity of the notch reflect normal coupling between cardiac function and systemic vascular resistance.

Poor Arterial Compliance

This arterial pressure waveform demonstrates reduced arterial compliance, resulting in faster pulse wave transmission and earlier return of reflected pressure waves. The result of the reflected waves is augmentation of peak systolic pressure and the earlier appearance of the dicrotic notch (left shift) on the tracing. The early dicrotic notch reflects the combined effects of aortic valve closure and altered wave reflection in a stiff arterial system, rather than a change in valve timing itself.

Diastolic Runoff

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Diastolic runoff refers to the decline in arterial pressure that occurs as ventricular ejection ends and blood continues to flow into the microcirculation during diastole.

This decline is governed by the arterial time constant (τ), the product of total peripheral resistance (TPR) and total arterial compliance (C). It describes how long pressure is maintained after systole.

Diastolic Runoff

  • A steep diastolic downslope indicates low vascular resistance or reduced compliance, as seen with vasodilators or septic shock.

  • A shallow diastolic decline occurs when vascular resistance is high, as in cardiogenic shock or sympathetic vasoconstriction.

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Thus, the contour of the diastolic runoff curve provides insight into vascular tone, arterial stiffness, and residual perfusion pressure during diastole.

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End-Diastolic Pressure = Diastolic Blood Pressure

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The end-diastolic pressure (EDP), or diastolic blood pressure (DBP) on the arterial tracing, represents the lowest point of arterial pressure just before the next ventricular contraction. It is a dynamic (rather than a static) variable, reflecting the interplay between vascular properties and cardiac timing.

DBP depends primarily on two factors:

  1. The arterial time constant (τ) — the product of total peripheral resistance (TPR) and total arterial compliance (TAC).

  2. The diastolic time — determined by heart rate (HR).

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A shorter diastolic interval, as seen in tachycardia, allows less time for pressure decay, leading to a higher DBP. Conversely, in bradycardia, the longer diastolic time permits greater runoff and a lower DBP.

Thus, beyond arterial resistance and compliance, heart rate plays a critical role in determining DBP by modulating the duration of diastolic pressure decay.

Diastolic Blood Pressure

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How the Pressure Waveform Changes Throughout the Arterial Tree

Moving distally:

  • The systolic upstroke becomes steeper.

  • The systolic peak appears higher.

  • The dicrotic notch occurs later in the cycle.

  • The diastolic runoff becomes lower.   

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These alterations produce pulse pressure amplification, a phenomenon where systolic pressure increases and diastolic pressure decreases as the wave travels away from the aortic root.

This amplification is primarily driven by increased wave reflection in smaller, less compliant peripheral arteries, which augment the forward wave and sharpen the systolic profile.

However… life’s not so simple, and sometimes the complex interactions between components of the vascular properties and the flow ejected from the heart can give some “bizarre” waveform patterns:

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As blood travels from the aorta toward the peripheral arteries, the pressure waveform undergoes distinct transformations due to progressive changes in impedance, arterial resistance, and wave reflection.

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