Impedance arterial

Sodium nitroprusside is used for the short-term control of severe hypertension and can improve cardiac function in patients with left ventricular failure see Chapter 34). Nitroprusside acts by releasing nitric oxide (NO). NO activates the guanylyl cyclase-cyclic GMP-PKG pathway, leading to vasodilation. The mechanism of release of NO likely involves both enzymatic and nonenzymatic pathways. Tolerance does not develop to nitroprusside. Nitroprusside dilates both arterioles and venules the hemodynamic response results from a combination of venous pooling and reduced arterial impedance. In subjects with normal left ventricular function, venous pooling affects cardiac output more than does the reduction of afterload cardiac output thus tends to fall. In patients with severely impaired left ventricular function and diastolic ventricular distention, the reduction of arterial impedance leads to a rise in cardiac output see Chapter 33). Sodium nitroprusside is a nonselective vasodilator, and regional distribution of blood flow is little affected by the drug. In... 

Maughan W.L., Sunagawa K., Burkhoff D., et al. 1984. Effect of arterial impedance changes on the end-systolic pressure-volume relation. Circ. Res. 54 595. 

TABLE 56.4 Characteristic Arterial Impedances in Some Mammals ... 

Rose, W. and Shoukas, A.A. 1993. Two-port analysis of systemic venous and arterial impedances. Am. J. Physiol. 265 Heart Circ. Physiol. 34) H1577. 

To answer the question of optimal matching between the ventricle and arterial load, we developed a framework of analysis which uses simplified models of ventricular contraction and arterial input impedance. The ventricular model consists only of a single volume (or chamber) elastance which increases to an endsystolic value with each heart beat. With this elastance, stroke volume SV is represented as a linearly decreasing function of ventricular endsystolic pressure. Arterial input impedance is represented by a 3-element Windkessel model which is in turn approximated to describe arterial end systolic pressure as a linearly increasing function of stroke volume injected per heart beat. The slope of this relationship is E. Superposition of the ventricular and arterial endsystolic pressure-stroke volume relationships yields stroke volume and stroke work expected when the ventricle and the arterial load are coupled. From theoretical consideration, a maximum energy transfer should occur from the contracting ventricle to the arterial load under the condition E = Experimental data on the external work that a ventricle performed on extensively varied arterial impedance loads supported the validity of this matched condition. The matched condition also dictated that the ventricular ejection fraction should be nearly 50%, a well-known fact under normal condition. We conclude that the ventricular contractile property, as represented by is matched to the arterial impedance property, represented by a three-element windkessel model, under normal conditions. 

The conversion of the arterial impedance property into an effectixr elastance can be done by first representing the arterial impedance by a three-element Windkessel model (consisting of R, C, and R) and then by manipulating the model equations to arrive at an approximation of arterial end-systolic pressure PJ as... 

The test proceeded as follows (Figure 2). We chose from the literature a set of R, C and R values as the normal canine arterial impedance parameters, imposed this control afterload on a given left ventricle at 4 end-diastolic volumes, and identified the and parameter values of the ESPVR of this ventricle. The... 

Figure 4. Equilibrium diagram for ventriculo-arterial coupling. See Figure 3 legend for explanation of the Ees and curves. Points 1 to 5 indicate equilibria between the ventricular pump performance and arterial impedance property under various conditions discussed in text. The ventricule is assumed to contract at a fixed end-diastolic volume of 35 ml...

SAGAWA In reference to Figure 3, given an end-diastolic volume the stroke volume depends upon end-systolic pressure. When the end-diastolic volume is between 30 and 40ml and arterial impedance is normal, the stroke volume is something like 15 ml, which is pretty close to half of the end-diastolic volume. Thus, the ej ection fraction seems to become 50% under the matched condition of E = which you can observe in normal dogs and patients. 

Figure A. Pressure-volume loops and isochrones obtained against constant arterial impedance for different preloads.

Cole, R.T., Lucas, C.L., Cascio, W.E. and Johnson, T.A. 2005. A Lab VIEW model incorporating an open-loop arterial impedance and a closed-loop circulatory system. A . Biomed. Eng. 33 1555-1573. 

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