448 HANDBOOK OF PHYSIOLOGY ^ CIRCULATION I 



P'essure-Tim Hg 

 ISO 



-< / second >- 



/5 cm 



FIG. 18. Pulse contours in a 24-year-old man who had aortic 

 regurgitation. Aortic and radial pressure pulses were recorded 

 simultaneously, utilizing strain gauges having equal sensitivi- 

 ties. Contours are characterized by low diastolic pressure and 

 wide pulse pressure. Radial upstroke is abrupt. Dicrotic halt of 

 aortic contour is slurred, and a well-detined postdicrotic wave 

 cannot be identified. 



ejects a larger systolic volume but delivers most of 

 this during the first half of ejection. The consequence 

 is that comparatively less remains to be expelled 

 during the latter half of systole, thus resulting in the 

 systolic drop of pressure in the central and peripheral 

 pulses. Another factor which acts to give a rapid 

 diastolic runoff" and a low diastolic pressure is vaso- 

 dilatation; the calculated systemic resistance in 

 patients with aortic insufficiency is usually a low 

 normal (120). 



The effective cardiac output is usually normal at 

 rest and as a rule rises with exercise in contrast with 

 that in aortic stenosis. This is accomplished at the 

 expense of increased ventricular work by increasing 

 the ejection volume by an amount equal to the 

 regurgitated blood. This volume is increased in part 

 by a prolonged period of systolic ejection resulting 

 from the shortened phase of isometric contraction. 

 In animal experiments an increased cardiac rate also 

 helps to maintain a normal cardiac output. Gorlin 

 and colleagues (120) confirmed this in man and 

 pointed out that an increase in heart rate resulted in 

 a decrease in the amount of blood regurgitated and, 

 as a result, in an increase in diastolic pressure. 



The increased diastolic blood volume and intra- 

 ventricular tension in the left ventricle lead to en- 

 largement of that chamber. Rosenbach (200), who 

 first produced aortic insufficiency in rabbits, noted an 

 initial dilatation followed by hypertrophy of the left 

 ventricle. In human aortic insufficiency, dilatation 



and hypertrophy of the left x'entricle are invariably 

 found in patients with significant aortic regurgitation. 

 Failure of the left ventricle in aortic insufficiency 

 usually occurs after a relatively long period of perfect 

 or near perfect compensation. Left \entricular failure 

 is associated with dilatation of that chamber and of 

 the mitral orifice with consequent functional mitral 

 regurgitation. Left-sided heart failure then results in 

 pulmonary congestion and eventually in right-sided 

 heart failure similar to that in mitral-\alve disease. 



MITRAL STENOSIS. This Icsion is much more often 

 acquired than congenital. Congenital endocardial 

 stenosis of the left ventricle produces hemodynamic 

 effects in the pulmonary circulation and right ventricle 

 similar to those of mitral stenosis. Clinical mitral 

 stenosis is characterized by two pathognomonic signs: 

 the occurrence of a rumbling apical murmur some- 

 times combined with a thrill in mid-diastole or 

 presystole, and left atrial and right ventricular en- 

 largement. The alterations in the dynamics of the 

 circulation depend on the degree of stenosis and not 

 infrequently on the onset of atrial fibrillation. 



In circulation models containing both a greater 

 and a lesser circuit, the production of a severe mitral 

 stenosis causes a decreased systolic output, a reduction 

 in arterial pressure, an accumulation of blood in the 

 left atrium and its tributary veins, and an increase in 

 mean pressure in the pulmonary artery. Since the 

 venous return is automatically diminished in such a 

 system, venous pressure falls, the right ventricle fills 

 less completely, and its output is diminished (261). 

 Most of the experimental work on animals has done 

 little more than to confirm these results. The essential 

 changes in ventricular filling were described by 

 Hirschfclder (132). Mild stenosis affects chiefly the 

 rapid inflow, but this reduction of filling can be 

 overcome by the action of an increased atrial con- 

 traction toward the end of diastole. When stenosis is 

 severe, however, the flow during early diastole is 

 greatly reduced, whereas the augmented atrial con- 

 traction is unable to drive any considerable volume 

 through the narrowed valve and as a consequence 

 systolic discharge diminishes. 



The maintenance of blood flow through the 

 narrowed mitral orifice is determined by the excess of 

 left atrial over left ventricular pressure in diastole. 

 The left atrial and left ventricular pressure pulses in 

 a 49-year-old man with mitral stenosis are shown in 

 figure 19. The individual waves contained in the usual 

 left atrial pressure pulse are labeled. The terminology 



