Objective: Pressure waves in the aorta can be described as the summation of forward pressure wave generated by ventricular contraction and backward wave. Backward wave is usually regarded as being due to reflections from discontinuities in the arterial tree but could arise as a result of wave emptying backwards from “reservoir”. We examined these possibilities in numerical models and with clinical data obtained during modulation of ventricular and arterial function using inotropic, vasodilator and vasopressor drugs.

Methods: Numerical models included simple Windkessel models with no wave propagation and a distributed single tube model terminated with impedance which allows wave propagation. Clinical data was obtained by carotid tonometry and Doppler sonography during modulation of cardiovascular function in healthy volunteers with dobutamine (2.5 – 7.5 μg/Kg/min), norepinephrine (12.5 – 50 ng/Kg/min), phentolamine (10 – 40 μg/min) and nitroglycerin (0.03 – 0.30 μg/min). Wave intensity analysis and arterial reservoir theory were applied to numerical models and clinical data.

Results: For numerical modelling, backward pressure over a range 0 – 50 mmHg was highly correlated with reservoir pressure both in Windkessel (R=0.958, P<0.001) and single tube models (R=0.990, P<0.001). For clinical data, there was a linear relationship between backward pressure over a range 5 – 20 mmHg and reservoir pressure (R=0.911, P<0.001) for all the subjects at rest and after inotropic/vasomotor stimulation. Augmentation pressure was neither related to the reflected pressure, nor to the reservoir pressure.

Conclusion: This study shows that the backward pressure wave may arise in large part from an arterial reservoir.