PHYSIOLOGIC CONSEQUENCES OF CONGENITAL HEART DISEASE 



447 



VALVULAR AORTIC STENOSIS 

 ( cf- 12 years } 



Pressure — mn 

 150 



LEFT RADIAL 

 ARTERY 100 



SUBVALVULAR AORTIC STENOSIS 

 ( cf -14 years) 



Pressure -iDtn Hg 



ZOO ^ 



50 10° 



LEFT , 



VENTRICLE 



EFT RADIAL 

 ARTERY 



PULMONARY 

 ARTERY 



50 



LEFT ATRIUM 

 30 



ECG 

 Base Line 



FIG. 17. Pulse contours in valvular aortic stenosis compared with those in subvalvular aortic 

 stenosis. Simultaneously measured radial, aortic, left ventricular, and left atrial pressures were 

 recorded during percutaneous catheterization of left side of heart. Left ventricular systolic pressure 

 is 125 to 150 mm of mercury greater than aortic systolic pressure in both patients, indicating severe 

 obsti'uction to left ventricular outflow. Pronounced anacrotism of both radial pulse contours is 

 evident. However, aortic pressure pulse in patient with subvalvular aortic stenosis resembles normal 

 aortic contour. In addition, a small central postdicrotic wave is easily identified. 



and coronary inflow probably could not increase 

 beyond the limit reached at rest, and hence no more 

 work would be done. 



Decreases in peripheral vascular resistance and 

 dilatation from various causes, such as exercise, in 

 association with a fixed minute output that patients 

 with aortic stenosis have, are felt to be the basis for 

 the effort syncope these patients often experience 

 (120). Also, coronary insufficiency that is frequently 

 found in association with aortic stenosis may be the 

 result of a temporary increase in the disproportion 

 between left ventricular work load and coronary 

 flow, and of acute hypotension from systemic vaso- 

 dilatation. 



Further discussion of studies on aortic stenosis in 

 experimental animals will be found in the work by 

 Wiggers (262) and in Chapter 20, which gives a 

 detailed discussion of stenosis and incompetence of 

 all the intracardiac valves. 



AORTIC REGURGiT.ATioN. Purc aortic insufficiency is 

 rarely encountered as a congenital lesion. Studies of 

 the effects of acquired insufficiency help in under- 

 standing the congenital lesion, although the latter is 

 usually in combination with septal defects which are 

 responsible for the major hemodynamic alterations. 



Insufficiency of the aortic semilunar valve results in 

 backflow or regurgitation of blood into the left 

 ventricle during diastole. Blood so regurgitating 



competes for space with the normal inflow through 

 the mitral orifice. Experimental work by Wiggers & 

 Maltby (264) in 1931 demonstrated that the magni- 

 tude of the backflow depends chiefly on the size of the 

 leak and can range from 5 per cent with small leaks 

 to 50 per cent or more when the cusps are rendered 

 totally deficient in experimental animals. Gorlin 

 et al. (120) showed that regurgitant orifice areas of no 

 greater than 0.5 cm- were capable of more than 

 doubling total ventricular output and work. 



The simultaneously recorded pressure pulse curves 

 from the aorta and radial artery of a 24-year-old man 

 with aortic insufficiency are shown in figure 18. The 

 dicrotic halt of the aortic pulse contour is slurred and 

 a well-defined postdicrotic wave cannot be demon- 

 strated. There is a low diastolic pressure, and the 

 radial-artery upstroke is abrupt. 



The rapid rise and fall of the radial pulse wave 

 combined with its large amplitude are generally 

 ascribed to the rapid discharge of a large volume of 

 blood during systole and regurgitation of a consider- 

 able volume during diastole. As Wiggers pointed out, 

 however, measurements of the radial pulse curves 

 demonstrate that the chief collapse occurs during 

 systolic ejection, not during diastole. The reason for 

 this seems to be that both central and peripheral 

 pulses reach their maximum more rapidly than 

 normally. This is due to the fact that the ventricle 

 under greatly increased initial tension not only 



