Pressure and blood flow measurements in the ascending aorta result from the interaction between the heart and arterial system. When LV pressure exceeds the aortic pressure, it becomes the driving force for the movement of blood into the ascending aorta.162 This driving force is dependent on the intrinsic contractility of ventricle muscle, the size and shape of the left ventricle, and the heart rate. It is opposed by several forces that impede the development of flow and are interrelated in a complex manner. Three major determinants of arterial impedance include (1) resistance, (2) inertia, and (3) compliance.
Resistance is related to blood viscosity and the geometry of the vasculature; it opposes flow and is unaffected by changes in heart rate. Inertia, which is related to the mass of the column of blood, opposes the rate of change of arterial blood flow (i.e., acceleration) and depends on the heart rate. Compliance is related to the distensibility of the vascular walls, opposes changes in arterial blood volume, and also depends on the heart rate. The heart rate dependency of inertia and compliance introduces phase shifts between instantaneous pressure and flow in a pulsatile system.167 Inertia and compliance are important determinants of the character of ventricular ejection, especially in early systole, when flows and pressures are changing rapidly.
The arterial pulse wave begins with aortic valve opening and the onset of LV ejection. Aortic pressure rises rapidly in early systole because the LV stroke volume enters the aorta faster than it flows to distal sites. The rapid-rising portion of the arterial pressure curve is often termed the anacrotic limb (from the Greek, meaning "upbeat"). In experimental animals and in humans, peak proximal aortic flow velocity occurs slightly earlier than peak pressure.167 After its peak, aortic pressure declines as ventricular ejection slows and peripheral blood flow continues. During isovolumic relaxation, a transient reversal of flow from the central arteries toward the ventricle just prior to aortic valve closure is associated with an incisura on the descending limb of the aortic pressure pulse. The subsequent smaller, secondary positive wave has been attributed to the elastic recoil of the aorta and aortic valve but is partially due to reflected waves from more distal arteries. Subsequently, aortic pressure decreases again as further "runoff" in the peripheral circulation occurs in diastole.
The proximal aortic pulse pressure is directly proportional to the ratio of stroke volume to arterial distensibility, but multiple factors influence this complex relationship.171 Arterial distensibility diminishes as the distending arterial pressure increases. Accordingly, the pulse pressure for a constant stroke volume will be larger if the mean blood pressure is elevated. In addition, arterial distensibility varies inversely with the rate of rise of intraluminal pressure. When the systolic ejection rate increases, the stiffer arterial wall results in a greater pulse pressure. Finally, the arterial pulse pressure is modified by reflected pressure waves and by the rate of blood flow from arterioles to veins.
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