Vascular load defined by the aortic input impedance spectrum.
The load that the arterial system places upon the myocardium during ventricular ejection is of primary importance in the consideration of ventricular function. This dynamic load can be characterized by the total aortic input impedance spectrum obtained from Fourier analysis of pulsatile pressure and flow waves recorded in the ascending aorta. Certain indices derived from the impedance spectrum provide quantitative and qualitative information about this dynamic load in terms of peripheral arteriolar dimensions (resistance), aortic wall stiffness (compliance), and wave reflections (reflectance). Studies in isolated heart preparations and intact dogs have shown that increases in resistance (decrease in arteriolar caliber) or aortic stiffness (decrease in aortic compliance) independently influence an increase in peak left ventricular pressure and a decrease in stroke volume. An increase in wave reflections also has the potential to reduce stroke volume while increasing peak pressure. Recent human studies have shown that in heart failure patients the components of the dynamic vascular load are also elevated compared to subjects without heart failure. Infusion of the vasodilator sodium nitroprusside abruptly reduces these components of vascular load as ventricular stroke output is enhanced. Thus, there is sufficient evidence to indicate that changes in the mechanical properties of the arterial tree influence the opposition to ventricular outflow. Since these properties can be described by the aortic input impedance spectrum, this function can be used to define the external load imposed on the ventricle by the vascular system.
D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology*; D003326:Coronary Circulation; D004285:Dogs; D006321:Heart / Q000502:physiology*; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology; D006339:Heart Rate; D006801:Humans; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D009599:Nitroprusside / Q000627:therapeutic use; D011312:Pressure; D013318:Stroke Volume; D014655:Vascular Resistance; D016276:Ventricular Function
D009599:Nitroprusside